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Beyond Long COVID – How reinfections could be causing silent long-term organ damage
David Putrino ❂ Sonya Buyting ~ Radio-Canada / Canadian Broadcasting Corporation • 20 March 2025
CBC Radio-Canada interview with long COVID [PASC] researcher David Putrino from the Icahn School of Medicine at Mount Sinai in New York.
📖 (20 Mar 2025 ~ Radio-Canada / Canadian Broadcasting Corporation) ‘Beyond long COVID – how reinfections could be causing silent long-term organ damage’.
© 2025 Radio-Canada / Canadian Broadcasting Corporation (CBC).
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❦ Radio interview ~ ‘Beyond long COVID – how reinfections could be causing silent long-term organ damage’
David Putrino interviewed by Bob McDonald.
Produced by Sonya Buyting for the Canadian Broadcasting Corporation (20 Mar 2025)
❦ ‘COVID may no longer be considered an official global emergency, but mounting scientific evidence suggests every COVID infection a person gets increases their risk of developing long-term health issues.
The long-term effects can show up as long COVID, with symptoms such as shortness of breath, digestive problems, fast or irregular heartbeats, extreme fatigue and ‘brain fog’, or as silently-accumulating cellular or organ damage.
“There is no such thing as a COVID infection without consequence,” says long COVID researcher, David Putrino, from the Icahn School of Medicine at Mount Sinai in New York.
Putrino has been studying the lingering effects of COVID since early in the pandemic five years ago.
“There is more and more literature emerging to show that, beyond long COVID, there are also effects that SARS-CoV-2 infections are having on the bodies of the general public that manifest in a way that might be viewed as silent. So what I mean by that is no-one’s going to their doctor and saying “I feel different” or “I feel as though my functional status has changed,” but what’s happening is, silently in the background, things are changing.
A good example of that is the effect that SARS-CoV-2 infections can have on cognition.
“There was a recent 2024 study showing us that individuals who survive an acute COVID-19 infection – these are not individuals who are getting diagnosed with long COVID – on average will lose somewhere in the neighbourhood of two to six IQ points per infection.”
So there is a cumulative effect that can be occurring with each infection.
Early in the pandemic, we actually published a paper where we showed that, even in animal models — when we infected mice with a very, very mild case of SARS-CoV-2 infection — which only caused lung inflammation, we still saw these inflammatory chemicals called chemokines emerging from the infected lungs and starting to attack central nervous system structures such as the spinal cord and the brain.
“This is a virus that, once it enters the body, is very capable of entering the bloodstream, creating immune responses that travel all over the body.”
In all of the peer-reviewed literature that has emerged on long COVID, we’ve seen that it is a very diffuse clinical syndrome where every single organ system can be affected. And at last count, over 200 symptoms have been catalogued as potential symptoms of long COVID.
When we actually dig into the science of why long COVID is causing the symptoms that it’s causing, we see that there are problems such as what we call ‘viral persistence’.
Meaning the SARS-CoV-2 virus is not being effectively cleared by the body and it’s sticking around.
It’s hiding out in different areas of the body in what we typically call ‘immune privileged sites’, which mean that immune cells don’t actually go there and can’t ‘seek out’ and destroy the virus. That can happen in a number of different locations in the body, which leads to a wide array of symptoms.
We also see that the virus can cause prolonged chronic inflammation that can be whole-body wide. So it can affect every single organ and so often, many of the symptoms that people are experiencing are more related to which organ is most susceptible to them given their past medical history.
We see things that are quite insidious. People who were pre-diabetic are suddenly diabetic. People who were having a few issues with their gallbladder suddenly can’t digest fat anymore.
In 2021, two colleagues of mine published a really wonderful paper that I think is very prescient and it spoke about why SARS-CoV-2 presents such an increased threat to cause persistent symptoms. The reality of that situation is that this virus has a lot of very unique qualities that specifically cause immune damage to the host.
So it’s not just about infecting you and causing respiratory illness and fever, and all of the things that we usually get with the viral infection. This virus also specifically causes your immune system to become weaker.
“This virus also specifically causes your immune system to become weaker.”
It disrupts what we call ‘interferon signalling’, which is part of the immune system that helps you to fight off infections or latent infections, such as Epstein Barr virus.
Typically our immune system can keep these things suppressed, but when SARS-CoV-2 enters the picture, it starts to cause altered interferon signalling. It causes immune damage and dysregulation.
And suddenly, not only does your body have trouble clearing the SARS-CoV-2 virus itself, but it also starts to have trouble keeping some of these other viruses that have been latent from reactivating and causing problems.
In addition to SARS-CoV-2’s ability to dysregulate the immune system and suppress the immune system, the spike protein itself is very damaging to blood vessel structures as well as red blood cells and platelets themselves.
“And so between those two features, the ability to dysregulate the immune system and the ability to cause systemic damage throughout the bloodstream, you have a very dangerous novel virus on your hands.”
In 2023, we published a paper in Nature where we showed that individuals with long COVID were much more likely than a cohort of healthy controls to express signs of what we call ‘T-cell exhaustion’. Meaning that their T cells, which are parts of the immune system that are typically used to fight off infections, are starting to present as exhausted – that there has been a persistent stimulation of these T cells for long enough that their responses over time are starting to weaken.
As a result, in this study we saw immune dysregulation, we saw hormonal dysregulation, we saw reactivation of herpes viruses that were previously thought to be latent.
And as we have made leaps and bounds in our ability to understand the role of these persistent pathogens, these things that we used to think, “Everybody’s got Epstein-Barr virus, but don’t worry, it sort of just lays dormant in your body and it doesn’t cause any trouble.”
What we’re learning is that it very much can cause trouble. If it’s mixed with another pathogen [such as SARS-CoV-2], and that pathogen causes the reactivation, then people can get very, very sick.
For the longest time in the field of immunology, there was the sort of adage that your immune system needs to be tested every now and again to stay strong. That’s an old-fashioned idea.
The more new-fashioned and evidence-based idea is that, although your immune system can take on [a COVID] infection, you want to avoid testing it as much as possible because your body is sustaining damage with each infection that it survives.”
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📖 (20 Mar 2025 ~ Canadian Broadcasting Corporation) ‘Beyond Long COVID – How reinfections could be causing silent long-term organ damage ➤’.
© 2025 Radio-Canada / Canadian Broadcasting Corporation (CBC).
“If y’all are busy weakening your immune systems with one virus, let me assure you that there are packs of other pathogens out there waiting to chew on the leftovers.”
© 2023 Dr. Noor Bari (Emergency Medicine)
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❦ Related reading
📖 (xx xxx 202x ~ Pub) Link ➤➲
© 202x Author / Pub.
In process, 12 Apr 2025.
More... Reinfection & Immunity
‘ Vaccine effectiveness against SARS-CoV-2 [COVID-19] infection declines markedly with time and Omicron variants . ’
‘ While acute [short-term] symptoms of reinfection are generally milder, the severity and incidence rate of long COVID increase significantly with the number of reinfections . ’
‘ These findings have important implications for understanding the potential impact of COVID-19 on long-term immune function and susceptibility to pathogens . ’
‘Before Omicron, natural infection provided strong and durable protection against reinfection, with minimal waning over time. However, during the Omicron era, protection was robust only for those recently infected, declining rapidly over time and diminishing within a year.’
‘ Reinfection , which is now the dominant type of SARS-CoV-2 infection , is not inconsequential ; it can trigger de novo Long Covid or exacerbate its severity . Each reinfection contributes additional risk of Long Covid: cumulatively , two infections yield a higher risk of Long Covid than one infection , and three infections yield a higher risk than two infections .’
❦ ‘The occurrences of respiratory disorders among patients who survived for 30 days after the COVID-19 diagnosis continued to rise consistently, including asthma , bronchiectasis , COPD , ILD , PVD * , and lung cancer . * COPD = Chronic obstructive pulmonary disease . ILD = Interstitial lung disease . PVD = Peripheral vascular disease . With the severity of the acute phase of COVID-19, the risk of all respiratory diseases increases progressively. Besides, during the 24-months follow-up, we observed an increasing trend in the risks of asthma and bronchiectasis over time, which indicates that long-term monitoring and meticulous follow-up of these patients is essential. These findings contribute to a more complete understanding of the impact of COVID-19 on the respiratory system and highlight the importance of prevention and early intervention of these respiratory sequelae of COVID-19. In this study, several key findings have been further identified. Firstly, our research demonstrates a significant association between COVID-19 and an increased long-term risk of developing various respiratory diseases. Secondly, we found that the risk of respiratory disease increases with severity in patients with COVID-19, indicating that it is necessary to pay attention to respiratory COVID-19 sequelae in patients, especially those hospitalized during the acute stage of infection. This is consistent with the findings of Lam et al., who found that the risk of some respiratory diseases (including chronic pulmonary disease, acute respiratory distress syndrome and ILD) increased with the severity of COVID-19. Notably, however, our study found that asthma and COPD remained evident even in the non-hospitalized population. This emphasizes that even in cases of mild COVID-19, the healthcare system should remain vigilant. Thirdly, we investigated differences in risk across time periods, as well as the long-term effects of COVID-19 on respiratory disease. During the 2-years follow-up period, the risks of COPD, ILD, PVD and lung cancer decreased, while risks of asthma and bronchiectasis increased. Fourthly, our study showed a significant increase of the long-term risk of developing asthma, COPD, ILD, and lung cancer diseases among individuals who suffered SARS-CoV-2 reinfection. This finding emphasizes the importance of preventing reinfection of COVID-19 in order to protect public health and reduce the potential burden of SARS-CoV-2 reinfection. Interestingly, vaccination appears to have a potentially worsening effect on asthma morbidity compared with other outcomes. This observation aligns with some previous studies that have suggested a possible induction of asthma onset or exacerbation by COVID-19 vaccination. It suggests that more care may be necessary for patients with asthma on taking the COVID vaccines. The underlying mechanisms associated with COVID and respiratory outcomes are not fully understood, but several hypotheses have been proposed. First, SARS-CoV-2 can persist in tissues (including the respiratory tract), as well as the circulating system for an extended period of time after the initial infection. This prolonged presence of the virus could directly contribute to long-term damage of the respiratory tissues, consequently leading to the development of various respiratory diseases. Second, it has been observed that SARS-CoV-2 infection can lead to prolonged immunological dysfunctions, including highly activated innate immune cells, a deficiency in naive T and B cells, and increased expression of interferons and other pro-inflammatory cytokines. These immune system abnormalities are closely associated with common chronic respiratory diseases – asthma, bronchiectasis, COPD, as well as the development of lung cancer. Next, SARS-CoV-2 itself has been shown to drive cross-reactive antibody responses, and a range of autoantibodies were found in patients with COVID-19. In conclusion, our research adds to the existing knowledge regarding the effects of COVID-19 on the respiratory system. Specifically, it shows that the risk of respiratory illness increases with the severity of infection and reinfection. Our findings emphasize the importance of providing extended care and attention to patients previously infected with SARS-CoV-2.’ ❂ 📖 (17 Feb 2024 ~ The Lancet: eClinical Medicine) Long-term risks of respiratory diseases in patients infected with SARS-CoV-2: a longitudinal, population-based cohort study ➤ © 2024 The Lancet: eClinical Medicine .
“I would argue that COVID-19 is not a disease of the lungs at all. It seems most likely that it is what we call a vascular and neurologic infection, affecting both nerve endings and our cardiovascular system.”
❦ Chris Whitty, from the Covid Inquiry: “The one situation... that you would ever aim to achieve herd immunity is by vaccination . That is the only situation that is a rational policy response.” And yet... the UK is no longer offering vaccines to the vast majority of its working-age population. According to the JCVI member Dr Adam Finn, the UK’s strategy going forward is that: “... most under 65’s will now end up boosting their immunity not through vaccination, but through catching Covid many times .” ➲ (24 Sep 2023 ~ BBC) What you need to know about Covid as new variant rises ➤ Let me translate: The stated aim is to get infected over and over and over again... to protect against being infected over and over and over again! How does this make any sense at all? The government has decided that it is not good “value for money” to actually give the boosters out – even for the age groups who have already had Covid vaccine doses purchased for them (for example, the 50-65 year olds) – so millions of doses [8.5 million] are now destined to be binned, rather than being used. ➲ ‘COVID VACCINE: COST EFFECTIVENESS ASSESSMENT. For the first time ever, the UK government has used a ‘bespoke, non-standard cost-effectiveness assessment’ to decide who would be eligible for the Covid booster this Autumn. In this thread, I explore how this assessment was undertaken…’ ➤ Meanwhile, in many other countries, the booster is open to anyone who wants it . No strict eligibility criteria. Just step forward and get protected. Let’s take a look at a few: 1. THE USA : Covid booster available to EVERYONE aged 6 months and older. The CDC (USA’s Centers for Disease Control ) recommends that everyone ages 6 months and upwards get the updated COVID-19 booster to protect against serious illness. The new vaccine targets the most common circulating variants, and should be available later this week. The full details are here ➤ . 2. CANADA : Covid booster available to EVERYONE aged 6 months and older. Full details are here ➤ . 3. FRANCE : Covid booster available to EVERYONE. Full details are here ➤ . 4. BELGIUM : Covid booster available to EVERYONE. Full details are here ➤ . 5. JAPAN : Covid booster available to EVERYONE aged 6 months and older. Full details are here ➤ . Why is the UK falling so far out of step with so many other countries on their Covid vaccine strategy? How can they justify binning millions of purchased vaccine doses when there are many people who would gladly take them? ➲ ‘So what’s going to happen to the millions of purchased doses which now won’t be used? Well, here’s the real kicker... it seems they’re destined for the bin. A number of alternative uses have been considered, but the conclusion is: “THESE DOSES HAVE NO FEASIBLE ALTERNATIVE USE”. ’ ➤ If the UK government won’t fund deployment of the Covid jab to EVERYONE (as so many other countries do), then why isn’t there at least an option to buy it privately? This model already exists with the flu jab – why is there not the same option for Covid? © 2023 Cat in the Hat ➲
❦ ‘The emergence of [new SARS-CoV-2 Variant of Interest] BA.2.86 meant a decision was made to bring forward the autumn Covid booster to better protect the most vulnerable this winter. But the new jabs are only available to people over 65 years old – it was the over-50s last year – and those with certain health conditions. That is a tactical decision , says Dr. Adam Finn, Professor of Paediatrics at the University of Bristol. He explained: “When younger people who’ve already had infections and vaccines get Covid [again], they get a cold and a cough and might be off work for a few days. There’s no real value in investing a lot of time and effort immunising them again when there are so many other things for the Health Service to be doing.” [ ❦ Note : Can a 62-year-old be defined as a ‘ younger person ’? Yes, at a pinch, if Mr. Finn compares them to a 78-year-old. What age-group do these ‘ younger people ’ belong to who don’t need vaccinating, and who instead need to be continually reinfected with a highly pathogenic Biohazard-Level 3 virus? Could it be a 32-year-old man or woman hoping to have a baby ? Or the 0 to 19-year-olds , who are the academic professor’s strong suit? ] ‘The reality is then that most under-65s will now end up boosting their immunity not through vaccination , but through catching Covid many times . In general, Prof Finn says each new infection should feel milder with the length of time you are sick reduced [sic] . “Each time you catch it, your immunity gets stronger and broader ,” he adds. ’ ❂ [ Note : This is simply not true, and is staggeringly dangerous. ] ❂ 📖 (24 Sep 2023 ~ Jim Reed, Health Reporter / BBC online) What you need to know about Covid as new variant [BA.2.86] rises ➤ © 2023 BBC .
❦ ‘The most common causes of acquired lymphocytopenia include: ➲ Protein-energy undernutrition. ➲ HIV infection. ➲ COVID-19 . ➲ Certain other viral infections. Patients with HIV infection routinely have lymphocytopenia, which arises from destruction of CD4+ T cells infected with the HIV virus. Patients with COVID-19 also frequently have lymphocytopenia ( 35% to 83% of patients ) . Lower lymphocyte counts portend a poor prognosis and an increased likelihood of requiring ICU admission and of dying from the disease. The cause of the lymphocytopenia is not completely understood, but COVID-19 can directly infect lymphocytes, and a cytokine-related apoptosis of the cells is likely. ➲ Lymphocytopenia is most often due to AIDS , and recently COVID-19 , or undernutrition, but it also may be inherited or caused by various infections, drugs, or autoimmune disorders. ➲ Patients have recurrent viral , bacterial , fungal , or parasitic infections .’ ❂ 📖 (Accessed 16 Sep 2023 ~ Merck & Co.) Entry for 'Lymphocytopenia' in Merck Manual ➤ © 2023 Merck & Co .
❦ ‘If y’all are busy weakening your immune systems with one virus, let me assure you that there are packs of other pathogens out there waiting to chew on the leftovers.’ © 2023 Dr. Noor Bari . ➲
❦ ‘Long COVID is the patient-coined term for the disease entity whereby persistent symptoms ensue in a significant proportion of those who have had COVID-19, whether asymptomatic, mild or severe. The disease burden spans from mild symptoms to profound disability, the scale making this a huge, new healthcare challenge. Long COVID will likely be stratified into several more or less discrete entities with potentially distinct pathogenic pathways. The evolving symptom list is extensive, multi-organ, multisystem and relapsing–remitting, including fatigue, breathlessness, neurocognitive effects and dysautonomia. A range of radiological abnormalities in the olfactory bulb, brain, heart, lung and other sites have been observed in individuals with Long COVID. Some body sites indicate the presence of microclots; these and other blood markers of hypercoagulation implicate a likely role of endothelial activation and clotting abnormalities. Diverse auto-antibody (AAB) specificities have been found, as yet without a clear consensus or correlation with symptom clusters. There is support for a role of persistent SARS-CoV-2 reservoirs and/or an effect of Epstein-Barr virus reactivation, and evidence from immune subset changes for broad immune perturbation. The oncoming burden of Long COVID faced by patients, healthcare providers, governments and economies is so large as to be unfathomable, which is possibly why minimal high-level planning is currently allocated to it.’ ❂ 📖 (11 July 2023 ~ Nature Reviews: Immunology) The immunology of long COVID ➤ © 2023 Altmann et al / Nature.
❦ Prior to 2020, there were four endemic human coronaviruses – OC43, NL-63, 229E, and HKU1 – which were known to cause 10 to 15 percent of common colds – or the ‘Common Cold Coronaviruses’ (CCCs). From at least the 1970s, we’ve known that infection with these coronaviruses does not lead to lasting protection from reinfection – this is textbook knowledge. CCCs are not just colds – they can cause severe pneumonias, and exhibit a risk profile very similar to SARS-CoV-2 with age. If reinfection really did strengthen immunity against CCCs, then older people would be the least affected – because they would have been regularly infected with diverse variants of these viruses in their past. But that is not the case – and SARS-CoV-2 is not a CCC. SARS-CoV-2 has a wide array of accessory proteins that silence and disrupt our normal immune responses. As we get older, our immune systems start to lose their effectiveness – and we become more susceptible to disease. This process is called immunosenescence . Repeated exposure to a virus like SARS-CoV-2 is fast-tracking more people into immunosenescence at ever-earlier ages, with potentially serious repercussions for their health and longevity. SARS-CoV-2 is a particularly nasty virus that can also trigger the hyperactivation of our own immune systems to cause severe disease. Infection by SARS-CoV-2 has been shown to lead to an increase in autoantibodies and autoimmune disease. Approximately 25 percent of people who develop an autoimmune disease will experience multiple autoimmune syndrome, and will risk a cascade of autoimmune conditions. SARS-CoV-2, like its 2002 predecessor SARS-CoV-1, is both a respiratory and a systemic virus, with an extremely broad cell-type and tissue-tropism covering nearly the whole body. Its ability to infect and do damage to lungs, hearts, kidneys, cardiovascular systems and brains is particularly well-documented. If each subsequent infection results in additional internal organ and immune-system damage, then at some point the damage accumulated – together with the accelerated immune-system aging and normal aging processes – can reasonably be expected to outweigh the protective benefits of immunity developed from previous infections. SARS-CoV-2 reinfects more frequently than influenza or the common cold, infects a wider range of organs, does more damage and seems capable of persisting in a range of organs. So if SARS-CoV-2 behaves like a textbook virus – but does more damage more quickly and more regularly – at what point does the body reach its tipping point? ❂ There are two versions of this article: a 7-minute read in simplified language ; and the full editorial version complete with references, which is an 18-minute-read and aimed towards the medical and scientific communities . ❦ 7-minute primer ~ ‘SARS-CoV-2 and “Textbook” Immunity’ ➤ ❦ Full 18-minute editorial ~ ‘SARS-CoV-2 and “Textbook” Immunity’ ➤ ❂ 📖 (5 May 2023 ~ The John Snow Project) SARS-CoV-2 and "Textbook" Immunity ➤ © 2023 The John Snow Project.
❦ Critically ill COVID-19 patients are highly susceptible to opportunistic fungal infection due to many factors, including virus-induced immune dysregulation , host-related comorbidities, overuse and misuse of antibiotics or corticosteroids, immune modulator drugs, and the emergencies caused by the pandemic. Fungal coinfection is a common complication of critically ill COVID-19 patients admitted to the ICU. Candidiasis , aspergillosis , and mucormycosis are the most common COVID-19-associated fungal infections and have a great impact on mortality rates . ❂ 📖 (18 Apr 2023 ~ BMC Infectious Diseases) Fungal infection profile in critically ill COVID-19 patients: a prospective study at a large teaching hospital in a middle-income country ➤ © 2023 Negm et al / BMC Infectious Diseases.
❦ ‘COVID-19 patients have a hypercoagulability state, and thrombosis is a life-threatening complication of them.’ ✻ Hypercoagulability , also known as thrombophilia , is a condition in which there is an abnormally increased tendency towards blood clotting . ‘From the early days of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) outbreak to the present, clinical and basic studies have indicated that coronavirus disease 2019 (COVID-19) may be associated with coagulopathy ( CAC ), which is involved in its related morbidity and mortality. Deep vein thrombosis ( DVT ) and pulmonary embolism ( PE ) are common in COVID-19 patients and are remarkably high in the intensive care unit (ICU)–admitted patients. CAC can lead to the formation of circulating microthrombi and macrothrombi which can involve multiple sites, including the lungs , brain , heart , and visceral organs like kidneys and spleen . There is a close relationship between the immune system and coagulation. The components of the hemostatic system play a role in the body’s immunity, and the activation of the immune system strongly influences the hemostatic system. Abnormal activation of the immune system may promote the growth of pathologies associated with thrombosis. COVID-19 is accompanied by an immune-cell hyperactivation and excessive production of proinflammatory cytokines , known as “ cytokine storm ”. CAC is theorized to result from dysregulated interactions between the immune and coagulation systems .’ ❂ 📖 (19 Apr 2023 ~ Annals of Hematology) Status of major hemostatic components in the setting of COVID-19: the effect on endothelium, platelets, coagulation factors, fibrinolytic system, and complement ➤ © 2023 Annals of Hematology .
❦ 'The risk of herpes zoster (HZ) [ shingles ] remained significantly higher [ +60% ] in patients with COVID-19, compared with those without COVID-19. The higher risk of HZ in the COVID-19 cohort compared with that in the non-COVID-19 cohort remained consistent across subgroup analyses regardless of vaccine status, age, or sex. The risk of HZ within a 12-month follow-up period was significantly higher in patients who had recovered from COVID-19 compared with that in the control group.' ❂ 📖 (18 Apr 2023 ~ Journal of Medical Virology) Long-term risk of herpes zoster following COVID-19: A retrospective cohort study of 2 442 686 patients ➤ © 2023 Journal of Medical Virology.
❦ The full picture of post-COVID-19 autoimmune diseases and their prevalence is lacking despite numerous case reports and small series. Two studies that use large cohorts now highlight that SARS-CoV-2 infection is linked to a substantially increased risk of developing a diverse spectrum of new-onset autoimmune diseases . The reports by Chang et al and Tesch et al provide a comprehensive overview of diverse new-onset autoimmune conditions after COVID-19. In addition, an earlier preprint of a retrospective matched cohort analysis using data from the Clinical Practice Research Datalink Aurum database of 458,147 SARS-CoV-2-infected and 1,818,929 uninfected adults across England between 31 January 2020 and 30 June 2021 reported that the incidence of type 1 diabetes mellitus , inflammatory bowel disease and psoriasis are significantly associated with SARS-CoV-2 infection. Some of the earliest evidence that SARS-CoV-2 infection leads to dysregulated immune responses came from paediatric patients who presented with multisystem inflammatory syndrome in children (MIS-C) , which, as the name indicates, involves diffuse organ system involvement and a clinical spectrum that overlaps with other hyperinflammatory syndromes , such as Kawasaki disease , toxic-shock syndrome , and macrophage activation syndrome . Since the start of the pandemic, many researchers have also reported isolated cases of adults with various post-COVID-19 autoimmune conditions. ❂ 📖 (12 Apr 2023 ~ Nature Reviews: Rheumatology) High risk of autoimmune diseases after COVID-19 ➤ © 2023 Sharma & Jagadeesh / Nature.
‘We are entering a phase of long COVID and chronic disability.’ ❂ ❦ ‘As the numbers of hospitalizations and deaths are dropping, many individuals declare the pandemic all but over, comforted by the belief that infections are mild and less dangerous than the seasonal flu. However, the scientific literature these last few weeks has been filled with deeply concerning reports. We are entering a phase of long COVID and chronic disability. The number of COVID-19 cases in the United States is unknown since our case reporting system has become unreliable and substantially undercounts cases. In England, as of the week ending March 7, 2023, 1 in 40 people is positive for COVID-19 , and reinfections are frequently occurring. It is estimated that as of November 9, 2022, 94% of the U.S. population has been infected by SARS-CoV-2 , and 65% of the United States population has been infected multiple times . The odds of self-reported long COVID were 28% less after the second infection. Unfortunately, the damage of long COVID from a second infection adds to the first . One of the most concerning long-term effects of COVID-19 is immune dysfunction or hypofunction . Confirmatory research was reported this week, and summarized in a National Institute of Health news release which stated: ‘… findings suggest that SARS-CoV-2 infection damages the CD8⁺ T cell response , an effect akin to that observed in earlier studies showing long-term damage to the immune system after infection with viruses such as hepatitis C or HIV .’ The authors conclude that this dysfunction causes lasting damage and may ‘contribute to long COVID, perhaps rendering patients unable to respond robustly to subsequent infections by SARS-CoV-2 variants or other pathogens .’ * * 📖 (20 Mar 2023 ~ National Institutes for Health) SARS-CoV-2 infection weakens immune-cell response to vaccination ➤ These findings mirror those reported by Files et al who state: ‘Overall, expression of these activation and exhaustion markers indicated more severe immune dysregulation of CD8 ⁺ T cells in the hospitalized group.’ And they found that ‘ CD8⁺ T cell expression of exhaustion markers increased in non-hospitalized individuals over time ’. * * 📖 (4 Jan 2021 ~ Journal of Clinical Investigation) Sustained cellular immune dysregulation in individuals recovering from SARS-CoV-2 infection ➤ The authors’ finding of damage to the immune system “akin” to HIV is very concerning, as is the amplification of this result in the NIH news release. Infection Control Today previously reported that the probable cause of the surges in infections we are seeing is an immune dysfunction caused by COVID-19 . With minimal public health interventions, Sweden also experienced surges in respiratory syncytial virus (RSV) cases. Most recently, Sweden has undergone a significant surge in seasonal flu, with reports from the Public Health Agency of Sweden of unusually severe cases. These [Swedish influenza] cases have occurred in ‘... people under the age of 18 without underlying disease or condition, and have been very seriously ill with complications such as myocarditis or encephalitis.’ Other diseases are also rising , exemplified by reports of record-high severe Streptococcal infections and Candida auris . These spikes in infections caused by multiple pathogens are associated with the SARS-CoV-2 pandemic and the mounting evidence of post-COVID-19 immune dysfunction. Vaccinations can not only reduce the incidence of severe disease, but can also help to prevent long COVID, reducing the incidence by 30% to 40%. However, we have expressed concern regarding the bivalent booster’s effectiveness, and reported a rapid waning of booster-induced immunity in the elderly. [See Footnote.] Recently, researchers from the United States found that the relative bivalent booster effectiveness at 5 to 7 months in preventing hospitalizations relative to monovalent vaccine dosages (2, 3, or 4) was 42% and 59% compared to no vaccination. Using the third vaccine dose as a baseline, the UK Health Security Agency found that an additional (fourth) vaccine dosage had effectiveness against hospitalizations at 10 weeks of only 50% .’ Source: 📖 (21 Mar 2023 ~ Infection Control Today) COVID-19: Study Suggests Long-term Damage to Immune System ➤ ❂ Footnote: On waning vaccine effectiveness * ‘Vaccine effectiveness is an important point. Although much of the younger population received a get-out-of-hospital free card for the latest variant, senior citizens were in its crosshairs. During the last 6 months (since May of 2022), those over the age of 75 had a higher rate of hospitalizations than in the Delta surge; those between the ages of 65 and 75 had approximately the same. Both age groups continue to be at high risk for death and disability. However, data showed that for those 65 years of age and older, the monovalent vaccine’s (2 or more doses) effectiveness for preventing hospitalizations fell to 28% in less than a year. Results were worse for those individuals under 65 years – only 19%.’ * 📖 (24 Feb 2023 ~ Infection Control Today) How Soon Is Another Booster Needed? Durability of Vaccine-Induced Immunity ➤ ❂ © 2023 Infection Control Today . ➲
❦ Lymphopenia , particularly when restricted to the T-cell compartment, has been described as one of the major clinical hallmarks in patients with coronavirus disease 2019 ( COVID-19 ) and proposed as an indicator of disease severity. Although several mechanisms fostering COVID-19-related lymphopenia have been described, including cell apoptosis and tissue homing, the underlying causes of the decline in T-cell count and function are still not completely understood. Patients with COVID-19 had reduced thymic function that was inversely associated with the severity of the disease. Our data demonstrate that the human thymus is a target of SARS-CoV-2 and thymic function is altered following infection . Note: Lymphopenia (also called lymphocytopenia) is a disorder in which your blood doesn't have enough white blood cells called lymphocytes. Lymphocytes play a protective role in your immune system. ❂ 📖 (7 Feb 2023 ~ Journal of Allergy and Clinical Immunology) SARS-CoV-2 infection of thymus induces loss of function that correlates with disease severity ➤ © 2023 Rosichini e t al / Journal of Allergy and Clinical Immunology.
❦ ‘Children have largely avoided severe COVID-19 symptoms because they have a strong initial ‘innate’ immune reaction that quickly defeats the virus. But unlike those of adults, children’s immune systems don’t remember the virus and don’t adapt, so when they’re next exposed to SARS-CoV-2, their body still treats it as a new threat. “Because children haven’t been exposed to many viruses, their immune system is still ‘naive’. And because they don't develop memory T cells, they are at risk of getting sick when they become reinfected. With each new infectious episode as they get older, there is a risk of their T cells becoming ‘exhausted’ and ineffective, like the T cells in older people. The price that children pay for being so good at getting rid of the virus in the first place is that they don’t have the opportunity to develop ‘adaptive’ memory to protect them the second time they are exposed to the virus,” says Professor Tri Phan.’ ❂ 📖 (26 Jan 2023 ~ Medical Life Sciences) Children's immune systems do not develop 'adaptive' memory to protect against second-time SARS-CoV-2 infection ➤ 📖 (January 2023 ~ Clinical Immunology) Tracking the clonal dynamics of SARS-CoV-2-specific T cells in children and adults with mild/asymptomatic COVID-19 ➤ © 2023 Emily Henderson / Medical Life Sciences.
❦ Fungi such as Aspergillus are so common in our surroundings that we breathe in hundreds to thousands of spores every day. In healthy people, fungi typically pose no threat, but they can cause deadly infections in those with compromised immune systems. However, it is increasingly recognized that viral infections such as influenza or SARS-CoV-2 can increase the risk of invasive Aspergillus infections even in healthy people. ❂ 📖 (12 Jan 2023 ~ News-Medical.Net) New insights into deadly fungal invasion in people with compromised immune systems ➤ © 2023 Emily Henderson / News Medical Life Sciences.
❦ Evolving research says COVID leaves many people at heightened risk for other infections. SARS-CoV-2 depletes the body’s supply of T-cells, * leaving young and old alike vulnerable to secondary infections. * (T-cells are the ‘front-line soldiers’ of the immune system, and the number of T-cells typically increases when the body is fighting off an infection.) “Individuals who are infected with COVID have many fewer T-cells – that’s a problem for us, because T-cells are a really important part of our immune system that helps defend us against infection.” But at least three studies show ✢ that COVID kills off a significant number of the body’s T-cells – so even when someone recovers from COVID, they are at a heightened risk for other viral, bacterial and fungal infections. “With the loss of these T-cells, we are now more vulnerable to all of these other infections, other viruses, other bacteria.” COVID-19 sparks what is called ‘programmed cell death’ among T-cells. Cells in the human body do this naturally as they age, but COVID-19 causes healthy T-cells to die that would otherwise be available to fight off infections. Many people who have had COVID brush it off, saying it was no worse than a bad case of the flu. What they don’t know is that they are more vulnerable to secondary infections that may cause them to seek help at a hospital emergency ward. ❂ ✢ 📖 (11 Jan 2023 ~ Nature Reviews / Immunology) Innate immune evasion strategies of SARS-CoV-2 ➤ 📖 (13 Jan 2023 ~ Preprint) Structure-based discovery of inhibitors of the SARS-CoV-2 Nsp14 N7-methyltransferase ➤ 📖 20 Apr 2021 ~ Nature / Cell Death & Differentiation) SARS-CoV-2 spike protein dictates syncytium-mediated lymphocyte elimination ➤ ❂ 📖 (20 Dec 2022 ~ Waterloo Region Record) Immune systems seriously weakened by COVID ➤ © 2022 Terry Pender / Waterloo Region Record.
❦ While COVID-19 was originally characterized as hyperinflammatory in its pathophysiology, emerging evidence demonstrates the possibility of a strongly immunosuppressive phenotype in more critical disease states. While immune activation from neutrophils and complement may contribute to inflammatory damage in the lungs, decreased antiviral responses, dysregulated macrophages and dendritic cells, and severe lymphopenia contribute to a suppressed state in which viral replication and secondary infections are prone. ❂ 📖 (6 Dec 2022 ~ Best Practice & Research Clinical Haematology) COVID-19 disease and immune dysregulation ➤ © 2022 Davitt et al / Best Practice & Research Clinical Haematology.
❦ ‘This morning someone said to me: — “I just can’t shake this... first a chest infection, and now a urine infection...” Someone else I know (very close) has had three eye infections post-COVID. Another has had a deterioration in their fertility, as compared to their baseline pre- and post-COVID. Measured. It’s almost as if the stuff in the science papers is real. None of them have twigged that COVID might have toasted them yet either. They are all heading into this next wave with no idea how dangerous it might be to abuse their already struggling immune system like this. You know what’s coming next... Multi-drug-resistant bacteria. Many are already here, but this is going to get really out of control. Trying to treat infections in immunodeficient patients is a great way to make loads of drug-resistant bacteria and viruses.’ ❂ 📖 (17 May 2024 ~ CIDRAP/University of Minnesota) Global Meta-analysis estimates 43% rate of multidrug resistance in COVID patients➤ 📖 (24 May 2023 ~ Current Microbiology) Interaction Between SARS-CoV-2 and Pathogenic Bacteria ➤ 📖 (18 Apr 2023 ~ BMC Infectious Diseases) Fungal infection profile in critically ill COVID-19 patients: a prospective study at a large teaching hospital in a middle-income country ➤ 📖 (29 Mar 2023 ~ Journal of Fungi) Fungal-Bacterial Co-Infections and Super-Infections among Hospitalized COVID-19 Patients: A Systematic Review ➤ 📖 (30 Sep 2021 ~ Insider) Drug-resistant infections in the US have risen sharply during the pandemic, and experts warn it's getting worse as COVID patients overwhelm hospital resources ➤ © 2022 Dr. Noor Bari, Emergency Medicine ➲
❦ ‘COVID-19 is fighting back by generally depressing the whole adaptive immune system. We are showing narrow resilience to COVID reinfections due to adapting – but we are becoming more vulnerable in general to infections of all kinds. ❦ Worst case scenario: a single infection causes on-going and progressive immunodeficiency . ❦ Best case scenario: a single infection causes temporary immunosuppression , and we suppress COVID transmission enough to allow recovery. ❦ Most likely scenario, medium-term: immunosuppression that becomes continuous and possibly progressive due to reinfections. Reduced immune function after a viral infection is not unusual. Many viruses do this. The concerning issue is the length and breadth of the immune system dysfunction, coupled with emerging evidence of other pathogens taking advantage.’ ❂ ❦ Immunosuppression ~ Suppression of the immune system and its ability to fight infection. ❦ Immunodeficiency ~ A state in which the immune system's ability to fight infectious diseases and cancer is compromised, or entirely absent. ❂ 📖 (13 Jan 2022 ~ Nature: Immunology) Immunological dysfunction persists for 8 months following initial mild-to-moderate SARS-CoV-2 infection ➤ © 2022 Dr. Noor Bari, Emergency Medicine ➲
❦ The 1918 influenza pandemic resulted in the loss of over 3% of the world’s population – at least 50 million people. But it wasn’t the flu virus that caused the majority of these deaths. An analysis of lung samples collected during that flu pandemic indicated that most of the deaths were likely due to bacterial pneumonia , which ran rampant in the absence of antibiotics. Even in more recent history, like the 1957 H2N2 and 2009 H1N1 flu pandemics , nearly 18% of patients with viral pneumonia had additional bacterial infections that increased their risk of death. And the COVID-19 pandemic is no different. ❂ 📖 (17 Aug 2022 ~ The Conversation) When COVID-19 or flu viruses kill, they often have an accomplice – bacterial infections ➤ © 2022 Hayley Muendlein / The Conversation.
❦ “So, we want to “live with the virus”. Is there any evidence of this occurring successfully anywhere? Yes! In bats... and it has taken 64 million years of evolution to get there. To “live with the virus”, bats have better host defences – they don’t overdo inflammation, and they can get rid of toxic compounds and deal with reactive oxygen species much better than humans. They literally live with the virus .
❦ While all viruses find ways to evade the body’s defenses, a growing field of research suggests that the coronavirus unhinges the immune system more profoundly than previously realized. Some Covid survivors have developed serious autoimmune diseases, which occur when an overactive immune system attacks the patient, rather than the virus. Doctors in Italy first noticed a pattern in March 2020, when several Covid patients developed Guillain-Barré syndrome, in which the immune systems attacks nerves throughout the body, causing muscle weakness or paralysis. As the pandemic has surged around the world, doctors have diagnosed patients with rare, immune-related bleeding disorders. Other patients have developed the opposite problem, suffering blood clots that can lead to stroke. All these conditions can be triggered by autoantibodies – rogue antibodies that target the patient’s own proteins and cells. ❂ 📖 (4 Mar 2021 ~ KFF Health News) Coronavirus Deranges the Immune System in Complex and Deadly Ways ➤ © 2021 Liz Szabo / KFF Health News.
More... PASC (‘Long Covid’)
‘ These findings have important implications for understanding the potential impact of COVID-19 on long-term immune function and susceptibility to pathogens . ’
‘ For patients already battling Alzheimer’s disease , studies indicate that Covid can exacerbate brain inflammation , damage immune cells , and accelerate the disease . Even previously healthy older adults face an increased risk of cognitive impairment and new-onset dementia after infection. Mild Covid cases in younger adults have also been linked to brain issues affecting memory and thinking . ’
‘But even people who had not been hospitalized had increased risks of many conditions, ranging from an 8% increase in the rate of heart attacks to a 247% increase in the rate of heart inflammation.’ Nature (2 Aug 2022) ‘Either symptomatic or asymptomatic SARS-CoV-2 infection is associated with increased risk of late cardiovascular outcomes and has causal effect on all-cause mortality in a late post-COVID-19 period.’ The American Journal of Cardiology (15 Sep 2023)
‘The proportions of PACS [PASC/Long Covid] patients experiencing chest pain, palpitation, and hypertension as sequelae were 22% , 18% , and 19% respectively.’
‘Scientists discover that even mild COVID-19 can alter brain proteins linked to Alzheimer’s disease, potentially increasing dementia risk. COVID-19-positive individuals exhibited lower cognitive test performance compared to controls – equivalent to almost two years of age-related cognitive decline. ’
‘The predominant symptoms , often clustering together, remain fatigue , cognitive disturbance and chest symptoms , including breathlessness , with sleep disorder and anxiety as additional complaints. Many patients with persistent PCS show impaired executive functioning , reduced cognitive processing speed and reduced physical exercise capacity .’
❦ On that 700-day cough... It’s a new thing, but it’s only reserved for inside supermarkets and offices. And pharmacies and hospitals and care homes. Oh, and your living-room. But apart from that, it’s not exactly a deal-breaker. I mean, c’mon. They put up with way worse in the 1900s. © 2024 C19.Life ❂
❦ ‘In this population of healthy young adult US Marines with mostly either asymptomatic or mild acute COVID-19, one fourth reported physical , cognitive , or psychiatric long-term sequelae of infection. The Marines affected with PASC [Post-Acute Sequelae of COVID-19 / Post-COVID-19 Complications / ‘Long Covid’] showed evidence of long-term decrease in functional performance suggesting that SARS-CoV-2 infection may negatively affect health for a significant proportion of young adults .’ ❂ ‘Among the 899 participants, 88.8% had a SARS-CoV-2 infection. Almost a quarter (24.7%) of these individuals had at least one COVID-19 symptom that lasted for at least 4 weeks meeting the a priori definition of PASC established for this study. Among those with PASC, 10 had no acute SARS-CoV-2 symptoms after PCR-confirmed infection suggesting that PASC can occur among asymptomatic individuals. Many participants reported that lingering symptoms impaired their productivity at work, caused them to miss work, and/or limited their ability to perform normal duty/activities. Marines with PASC had significantly decreased physical fitness test scores up to approximately one year post-infection with a three-mile run time that averaged in the 65th percentile of the reference cohort. [ PASC was associated with a significantly increased 3-mile run time on the standard Marine fitness test. PASC participants ran 25.1 seconds slower than a pre-pandemic reference cohort composed of 22,612 Marine recruits from 2016 to 2019. A three-mile run evaluates aerobic exercise , overhead lifting of an ammunition can and pull-ups evaluate strength , and shooting a rifle evaluates fine-motor skills .] Scores for events evaluating upper body (pull-ups, crunches, and ammo-can lift) were not significantly reduced by PASC; however, overall physical fitness scores were reduced. ‘The poorer run times and overall scores among PASC participants are indicative of on-going functional effects.’ Standardized health-based assessments for somatization, depression, and anxiety further highlighted the detrimental health effects of PASC. Almost 10% of participants with PASC had PHQ-8 scores ≥10. Increased somatization * has been associated with increased stress, depression, and problems with emotions. * [ Somatization / Somatisation = Medical symptoms caused by psychological stress.] Additionally, PASC participants had higher GAD-7 scores suggesting increased anxiety in a population with unique inherent occupational stressors associated with higher rates of anxiety, depression, and post-traumatic stress disorder. ‘Increased severity of anxiety among those with PASC, combined with greater rates of mental health disorders in general, could portend an ominous combination and should be closely followed.’ Like others, we identified cardiopulmonary symptoms as some of the most prevalent. The high prevalence of symptoms like shortness of breath, difficulty breathing, cough, and fatigue is particularly notable when combined with decreased objective measures of aerobic performance such as running. These results suggest pathology in the cardiopulmonary system. In contrast we observed no reduction in scores assessing strength and marksmanship suggesting the lack of detectable pathology in the neuro-musculoskeletal system. We have previously found in this same cohort that SARS-CoV-2 infection causes prolonged dysregulation of immune cell epigenetic patterns like auto-immune diseases. Based on the reported PASC symptoms, the potential current and future public health implications in this population could be substantial. ‘Chronic health complications from PASC, especially in a young and previously healthy population with a long life expectancy, could decrease work productivity and increase healthcare costs.’ Significant changes in the Years-of-Life lived with a disability can disproportionally increase disability-adjusted life-years, and should be considered when allocating resources and designing policy.’ ❂ 📖 (23 Oct 2024 ~ The Lancet: Regional Health/America) Clinical and functional assessment of SARS-CoV-2 sequelae among young marines – a panel study ➤ © 2024 The Lancet .
‘ Reinfection , which is now the dominant type of SARS-CoV-2 infection , is not inconsequential ; it can trigger de novo Long Covid or exacerbate its severity . Each reinfection contributes additional risk of Long Covid: cumulatively , two infections yield a higher risk of Long Covid than one infection , and three infections yield a higher risk than two infections .’
❦ This study confirms everything that I have seen in the microscope over the last few years. The authors of the study use a technique called dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI), an imaging technique that can measure the density, integrity, and leakiness of tissue vasculature. Comparing all individuals with previous COVID infection to unaffected controls revealed decreased general brain volume in patients with brain fog along with significantly reduced cerebral white matter volume in both hemispheres in the recovered and brain fog cohorts . Covid-19 induces brain volume loss and leaky blood-brain barrier in some patients. How can this be more clear? © 2024 Danielle Beckman. ➲ ❂ 📖 (22 Feb 2024 ~ Nature: Neuroscience) Blood–brain barrier disruption and sustained systemic inflammation in individuals with long COVID-associated cognitive impairment ➤ 📖 (22 Feb 2024 ~ Nature: Neuroscience) Leaky blood–brain barrier in long-COVID-associated brain fog ➤ ➲ Layperson overview: 📖 (February 2024 ~ Genetic Engineering and Biotechnology News) Leaky Blood Vessels in the Brain Linked to Brain Fog in Long COVID Patients ➤ Related: 📖 (7 Feb 2022 ~ Nature: Cardiovascular Research) Blood–brain barrier link to human cognitive impairment and Alzheimer’s disease ➤ ❂ © 2024 Nature .
❦ ‘The occurrences of respiratory disorders among patients who survived for 30 days after the COVID-19 diagnosis continued to rise consistently, including asthma , bronchiectasis , COPD , ILD , PVD * , and lung cancer . * COPD = Chronic obstructive pulmonary disease . ILD = Interstitial lung disease . PVD = Peripheral vascular disease . With the severity of the acute phase of COVID-19, the risk of all respiratory diseases increases progressively. Besides, during the 24-months follow-up, we observed an increasing trend in the risks of asthma and bronchiectasis over time, which indicates that long-term monitoring and meticulous follow-up of these patients is essential. These findings contribute to a more complete understanding of the impact of COVID-19 on the respiratory system and highlight the importance of prevention and early intervention of these respiratory sequelae of COVID-19. In this study, several key findings have been further identified. Firstly, our research demonstrates a significant association between COVID-19 and an increased long-term risk of developing various respiratory diseases. Secondly, we found that the risk of respiratory disease increases with severity in patients with COVID-19, indicating that it is necessary to pay attention to respiratory COVID-19 sequelae in patients, especially those hospitalized during the acute stage of infection. This is consistent with the findings of Lam et al., who found that the risk of some respiratory diseases (including chronic pulmonary disease, acute respiratory distress syndrome and ILD) increased with the severity of COVID-19. Notably, however, our study found that asthma and COPD remained evident even in the non-hospitalized population. This emphasizes that even in cases of mild COVID-19, the healthcare system should remain vigilant. Thirdly, we investigated differences in risk across time periods, as well as the long-term effects of COVID-19 on respiratory disease. During the 2-years follow-up period, the risks of COPD, ILD, PVD and lung cancer decreased, while risks of asthma and bronchiectasis increased. Fourthly, our study showed a significant increase of the long-term risk of developing asthma, COPD, ILD, and lung cancer diseases among individuals who suffered SARS-CoV-2 reinfection. This finding emphasizes the importance of preventing reinfection of COVID-19 in order to protect public health and reduce the potential burden of SARS-CoV-2 reinfection. Interestingly, vaccination appears to have a potentially worsening effect on asthma morbidity compared with other outcomes. This observation aligns with some previous studies that have suggested a possible induction of asthma onset or exacerbation by COVID-19 vaccination. It suggests that more care may be necessary for patients with asthma on taking the COVID vaccines. The underlying mechanisms associated with COVID and respiratory outcomes are not fully understood, but several hypotheses have been proposed. First, SARS-CoV-2 can persist in tissues (including the respiratory tract), as well as the circulating system for an extended period of time after the initial infection. This prolonged presence of the virus could directly contribute to long-term damage of the respiratory tissues, consequently leading to the development of various respiratory diseases. Second, it has been observed that SARS-CoV-2 infection can lead to prolonged immunological dysfunctions, including highly activated innate immune cells, a deficiency in naive T and B cells, and increased expression of interferons and other pro-inflammatory cytokines. These immune system abnormalities are closely associated with common chronic respiratory diseases – asthma, bronchiectasis, COPD, as well as the development of lung cancer. Next, SARS-CoV-2 itself has been shown to drive cross-reactive antibody responses, and a range of autoantibodies were found in patients with COVID-19. In conclusion, our research adds to the existing knowledge regarding the effects of COVID-19 on the respiratory system. Specifically, it shows that the risk of respiratory illness increases with the severity of infection and reinfection. Our findings emphasize the importance of providing extended care and attention to patients previously infected with SARS-CoV-2.’ ❂ 📖 (17 Feb 2024 ~ The Lancet: eClinical Medicine) Long-term risks of respiratory diseases in patients infected with SARS-CoV-2: a longitudinal, population-based cohort study ➤ © 2024 The Lancet: eClinical Medicine .
❦ Chronic disease is like the perfect medical crime. The cause is usually long gone by the time the disease manifests, and nobody links the two until it’s much too late for most. ❂ © 2024 Henry Madison . ➲
❦ It’s really not in the interest of the virus to kill us quickly. That’s why it has mutated to immune escape. That way it enters silently, and then eats you slowly whilst you’re still a spreading vector. Refrigerator trucks are long gone. That’s all the political class wanted. The unseen costs of CVD [cardiovascular disease] , DM [diabetes mellitus] , and both dementia and Parkinson’s Disease are the train coming down the tunnel. The economists are catching up. The actuaries are already there. Politicians and most people? Not yet... ❂ © 2024 Dr. David Joffe, PhD, FRACP / Respiratory Physician ➲ .
❦ ‘Although some studies have shown neuroimaging and neuropsychological alterations in post-COVID-19 patients, fewer combined neuroimaging and neuropsychology evaluations of individuals who presented a mild acute infection. Here we investigated cognitive dysfunction and brain changes in a group of mildly infected individuals. We conducted a cross-sectional study of 97 consecutive subjects ( median age of 41 years ) without current or history of psychiatric symptoms (including anxiety and depression) after a mild infection , with a median of 79 days (and mean of 97 days ) after diagnosis of COVID-19. We performed semi-structured interviews, neurological examinations, 3T-MRI scans, and neuropsychological assessments. The patients reported memory loss ( 36% ), fatigue ( 31% ) and headache ( 29% ). The quantitative analyses confirmed symptoms of fatigue ( 83% of participants), excessive somnolence ( 35% ), impaired phonemic verbal fluency ( 21% ), impaired verbal categorical fluency ( 13% ) and impaired logical memory immediate recall ( 16% ). Our group… presented higher rates of impairments in processing speed ( 11.7% in FDT- Reading and 10% in FDT- Counting ). The white matter (WM) analyses with DTI * revealed higher axial diffusivity values in post-infected patients compared to controls. * Diffusion tensor imaging tractography , or DTI tractography, is an MRI (magnetic resonance imaging) technique most commonly used to provide imaging of the brain. Our results suggest persistent cognitive impairment and subtle white matter abnormalities in individuals mildly infected , without anxiety or depression symptoms. One intriguing fact is that we observed a high proportion of low average performance in our sample of patients (which has a high average level of education ), including immediate and late verbal episodic memory, phonological and semantic verbal fluency, immediate visuospatial episodic memory, processing speed, and inhibitory control . Although most subjects did not present significant impaired scores compared with the normative data, we speculate that the low average performance affecting different domains may result in a negative impact in everyday life , especially in individuals with high levels of education and cognitive demands .’ ❂ ❦ Note how these findings might negatively affect daily activities that demand sustained cognitive attention and fast reaction times – such as driving a car or motorbike, or piloting a plane. Consider air-traffic control. Consider the impact on healthcare workers whose occupations combine long periods of intense concentration with a need for critical precision. ❂ 📖 (19 Jan 2024 ~ Nature: Scientific Reports) Microstructural brain abnormalities, fatigue, and cognitive dysfunction after mild COVID-19 ➤ © 2024 Nature .
‘ Clinical evidence suggests that SARS-CoV-2 may lead to hypocalcemia, altered bone turnover markers, and a high prevalence of vertebral fractures. ’
❦ ‘Acute infections with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cause a respiratory illness that can be associated with systemic immune cell activation and inflammation , widespread multi-organ dysfunction , and thrombosis . Not everyone fully recovers from COVID-19, leading to Long Covid, the treatment of which is a major unmet clinical need. Long Covid can affect people of all ages , follows severe as well as mild disease , and involves multiple organs . Patients with Long Covid display signs of immune dysfunction and exhaustion , persistent immune cell activation , and autoimmune antibody production , which are also pathological features of acute COVID-19. The complement system is crucial for innate immune defense by effecting lytic destruction of invading micro-organisms, but when uncontrolled, it causes cell and vascular damage . The complement cascade is activated by antigen–antibody complexes in the classical pathways or in the lectin pathway by multimeric proteins (lectins) that recognize specific carbohydrate structures, which are also found on the SARS-CoV-2 spike protein that facilitates host cell entry. Both pathways may contribute to the pronounced complement activation in acute COVID-19. Long Covid symptoms include a postexertional exhaustion reminiscent of other post-viral illnesses , such as myalgic encephalomyelitis ( ME ) – chronic fatigue syndrome ( MECFS ) with suspected latent viral reactivation . Antibody titer changes in Long Covid patients indicate an association of fatigue with reactivation of latent Epstein-Barr virus ( EBV ) infections , and Cervia-Hasler et al found that the severity of Long Covid symptoms is associated with cytomegalovirus ( CMV ) reactivation . A better understanding of the connections between viral reactivation, persistent interferon signaling, and autoimmune pathologies promises to yield new insights into the thromboinflammation associated with Long Covid. Although therapeutic interventions with coagulation and complement inhibitors in acute COVID-19 produced mixed results, the pathological features specific for Long Covid suggest potential interventions for clinical testing. Microclots are also observed in ME-CFS patients , indicating crucial interactions between complement, vWF, and coagulation-mediated fibrin formation in post-viral syndromes. A better definition of these interactions in preclinical and clinical settings will be crucial for the translation of new therapeutic concepts in chronic thromboinflammatory diseases .’ ❂ 📖 (18 Jan 2024 ~ Science) Immune damage in Long Covid ➤ © 2024 Wolfram Ruf / Science .
“I would argue that COVID-19 is not a disease of the lungs at all. It seems most likely that it is what we call a vascular and neurologic infection, affecting both nerve endings and our cardiovascular system.”
❦ ‘Alzheimer’s disease (AD) is acknowledged by the World Health Organisation (WHO) as a global public health concern. AD is the primary cause of dementia and accounts for 50–70% of cases. SARS-CoV-2 can damage the peripheral and the central nervous system (CNS) through both direct and indirect pathways, potentially leaving COVID-19 patients at higher risks for neurological difficulties, including depression, Parkinson’s disease, AD, etc., after recovering from severe symptoms. Patients who recovered from severe COVID-19 infection are more likely to acquire stable neuropsychiatric and neurocognitive conditions like depression, obsessive-compulsive disorder, psychosis, Parkinson’s disease, and Alzheimer’s disease. SARS-CoV-2 infection causes immune system dysfunction, which can lead to suppression of neurogenesis, synaptic damage, and neuronal death, all of which are associated with the aetiology of Alzheimer’s disease. Severe systemic inflammation caused by SARS-CoV-2 is predicted to have long-term negative consequences, such as cognitive impairment. Research has demonstrated that SARS-CoV-2-infected AD patients had a higher mortality rate. In a study from the Department of Neuroscience at the University of Madrid, 204 participants with Frontotemporal Dementia (FTD) and Alzheimer’s disease (AD) were enrolled. According to the study, 15.2% of these individuals had COVID-19 infection, and sadly, 41.9% of those who had the virus died as a result of their illness. COVID-19 causes a secondary effect on underlying brain pathologies, as SARS-CoV-2 has been shown to trigger or accelerate neurodegeneration processes that possibly explain long-term neurodegenerative effects in the elderly population. In response to the impact of COVID-19 in 2020, governments worldwide acted promptly by implementing various public health measures. During this period, people with cognitive impairments such as dementia or AD may have experienced greater stress and anxiety due to sudden changes in the environment and people’s behaviour. It is also significantly harder for AD patients to comprehend and execute defensive measures such as wearing face masks and sanitising frequently. ❂ COVID-19 has generated a worldwide outbreak, resulting in a slew of issues for humans, particularly those suffering from Alzheimer’s disease. Its ability to invade the central nervous system through the hematogenous and neural routes, besides attacking the respiratory system, has the potential to worsen cognitive decline in Alzheimer’s disease patients. The severity of this issue must be highlighted.’ ❂ 📖 (8 Jan 2024 ~ Frontiers in Aging Neuroscience) Unravelling the connection between COVID-19 and Alzheimer’s disease: a comprehensive review ➤ © 2024 Shajahan et al / Frontiers in Aging Neuroscience .
Post-exertional malaise (PEM) is a marked physical or mental fatigue and deterioration of symptoms occurring after physical , cognitive , social or emotional exertion that would have been tolerated previously. Symptoms typically worsen 12 to 48 hours after such activities , and can last for days , weeks or months , making it difficult to manage or predict. PEM is a hallmark symptom of myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS), and is commonly reported by people with Post-COVID-19 Syndrome (PCS/‘Long Covid’). PEM can be mitigated by activity management , or ‘ pacing ’.
❦ ‘Al-Aly’s study undertook a comparative analysis of 94 pre-specified health outcomes and found that over 18 months of follow-up, COVID was associated with a “ significantly increased risk ” for 64 of them, or nearly 70% . The disease’s enhanced risk list includes everything from cardiac arrest , stroke , chronic kidney disease , and cognitive impairment to mental health and fatigue , characteristics often associated with long COVID. By comparison, the seasonal flu was associated with increased risk in only 6 of the 94 conditions specified. Further, while COVID increased the risks for almost all the organ systems studied, the flu heightened risk primarily for the pulmonary ( lung ) system . Those findings, Al-Aly says, suggest that “ COVID is really a multi-systemic disease , and flu is more a respiratory virus ”.’ ❂ 📖 (14 Dec 2023 ~ Fortune) COVID-19 v. Flu: A ‘much more serious threat,’ new study into long-term risks concludes ➤ 📖 (14 Dec 2023 ~ The Lancet) Long-term outcomes following hospital admission for COVID-19 versus seasonal influenza: a cohort study ➤ © 2023 Carolyn Barber / Fortune .
❦ As a consequence of their occupation, doctors and other healthcare workers were at higher risk of contracting coronavirus disease 2019 (COVID-19), and more likely to experience severe disease compared to the general population. Post-acute COVID (Long COVID) in UK doctors is a substantial burden. Insufficient respiratory protection could have contributed to occupational disease, with COVID-19 being contracted in the workplace , and resultant post-COVID complications. Although it may be too late to address the perceived determinants of inadequate protection for those already suffering with Long COVID, more investment is needed in rehabilitation and support of those afflicted . ❂ 📖 (11 Dec 2023 ~ Occupational Medicine) Post-acute COVID-19 complications in UK doctors: results of a cross-sectional survey ➤
❦ 'For middle-aged adults ( 50–64 ) in this period [June 2022 – June 2023 ], the relative excess for almost all causes of death examined was higher than that seen for all ages .' ➲ ‘Since July 2020, the Office for Health Improvement and Disparities (OHID) has published estimates of excess mortality. In the period from week ending 3rd June 2022 to 30th June 2023 , excess deaths for all causes were relatively greatest for 50–64 year olds ( 15% higher than expected ), compared with 11% higher for 25–49 and < 25 year olds , and about 9% higher for over 65 year old groups. Several causes, including cardiovascular diseases , show a relative excess greater than that seen in deaths from all-causes ( 9% ) over the same period (week ending 3rd June 2022–30th June 2023), namely: all cardiovascular diseases ( 12% ), heart failure ( 20% ), ischaemic heart diseases ( 15% ), liver diseases ( 19%) , acute respiratory infections ( 14% ), and diabetes ( 13% ). For middle-aged adults (50–64) in this 13-month period, the relative excess for almost all causes of death examined was higher than that seen for all ages . Deaths involving cardiovascular diseases were 33% higher than expected, while for specific cardiovascular diseases, deaths involving ischaemic heart diseases were 44% higher , cerebrovascular diseases 40% higher and heart failure 39% higher . Deaths involving acute respiratory infections were 43% higher than expected and for diabetes , deaths were 35% higher . Deaths involving liver diseases were 19% higher than expected for those aged 50–64 , the same as for deaths at all ages. Looking at place of death, from 3rd June 2022 to 30th June 2023 there were 22% more deaths in private homes than expected compared with 10% more in hospitals . The greatest numbers of excess deaths in the acute phase of the pandemic were in older adults. The pattern now is one of persisting excess deaths which are most prominent in relative terms in middle-aged and younger adults , with deaths from CVD [cardiovascular] causes and deaths in private homes being most affected.’ ❂ ➲ [C19.Life Note ] : Considering their findings and conclusion, I’m not sure why the authors would choose to use the term ‘post-pandemic’ in this title – when their evidence points to an on-going pandemic, fueled by continuing high rates of infection, that is now simply killing younger age-groups than previously seen.] ❂ 📖 (1 Dec 2023 ~ The Lancet (Regional Health Europe) Excess mortality in England post Covid-19 pandemic: implications for secondary prevention ➤ © 2023 Pearson-Stuttard et al / The Lancet (Regional Health Europe) .
❦ SARS-CoV-2 infection precipitates a molecular cascade that reactivates latent viral agents. Infection doesn’t just pass through the body’s defenses but rather reprograms them. It reactivates dormant pathogens and perpetuates a cycle of chronic immune activation. Long COVID sufferers are burdened with a significantly higher prevalence of immune responses to certain DNA viruses – namely, Epstein-Barr Virus (EBV)* and Parvovirus B19 – than those in good health. * Epstein-Barr Virus (EBV) is a common human virus that spreads primarily through saliva. It is a member of the herpes virus family and is found all over the world. Most people will get infected with EBV in their lifetime and will not have any symptoms. Elevated levels of antibodies against these viruses in Long COVID patients not only signal potential viral reactivations. It also suggests a reality where SARS-CoV-2 may be inciting a smoldering activation of chronic viral infections. ❂ 📖 (9 Nov 2023 ~ European Heart Journal) Sequential activation of DNA viruses by the RNA virus SARS-CoV-2 in patients with long COVID syndrome ➤ © 2023 Outbreak Updates ➲
❦ ‘It is now well established that post-COVID syndrome ( PCS ) represents a serious complication in a substantial number of patients following SARS-CoV-2 infection. PCS is diagnosed when COVID-19-related symptoms persist for more than 3 months. It can occur even after an initially mild to moderate course of infection , and comprises a large variety of symptoms . Around 30% of PCS patients show neurological and neuropsychiatric sequelae , such as fatigue , depressive symptoms , and cognitive dysfunction . These are experienced as particularly debilitating, as they have detrimental effects on daily functioning in PCS patients and hamper a successful return to their jobs. Fatigue is a frequent and one of the most debilitating symptoms in post-COVID syndrome (PCS). Recently, we proposed that fatigue is caused by hypoactivity of the brain’s arousal network and reflected by a reduction of cognitive processing speed . Eighty-eight PCS patients with cognitive complaints and 50 matched healthy controls underwent neuropsychological assessment. Seventy-seven patients were subsequently assessed at 6-month follow-up. Patients showed cognitive slowing indicated by longer reaction times compared to control participants in a simple-response tonic alertness task and in all more complex tasks requiring speeded performance . Reduced alertness correlated with higher fatigue . Alertness dysfunction remained unchanged at 6-month follow-up and the same was true for most attention tasks and cognitive domains .’ ❂ 📖 (7 Nov 2023 ~ Journal of Neurology) Persistent cognitive slowing in post-COVID patients: longitudinal study over 6 months ➤ © 2023 Journal of Neurology .
➲ A layperson-level overview from New Atlas on how all variants of SARS-CoV-2 – the virus that causes COVID-19 – are ‘neuroinvasive’ , meaning that all can infect or enter the brain and the nervous system . ❂ ❦ ‘... We know COVID is associated with a variety of neurological symptoms , both short- and long-term, but it still isn’t entirely clear whether these cognitive issues are the result of the virus directly infecting brain cells or simply due to a broader systemic inflammatory response. Studies looking at human brain tissue have yielded contradictory results. Some have found direct traces of SARS-CoV-2 , while others report only inflammatory damage . Animal models certainly demonstrate it is possible for the virus to infect the brain, but human tissue samples are obviously taken after a patient dies – meaning researchers can only hypothesize what happens during an acute infection. Using a hamster model, the research compared infection with the original SARS-CoV-2 virus from 2020 to several subsequent variants including Gamma, Delta and Omicron/BA.1 variants. Interestingly, the findings confirmed epidemiological observations showing acute disease severity is reduced in Omicron infections – however, all [SARS-CoV-2] variants demonstrated similar neuroinvasive capabilities. And, most strikingly, all variants infected the brain’s olfactory regions regardless of whether symptoms of anosmia (the loss of sense of smell) were present or not. “This suggests that anosmia and neuronal infection are two unrelated phenomena. If we follow this line of reasoning, it is quite possible that even an asymptomatic infection is characterized by the spread of the virus in the nervous system.” The researchers conclude this suggests all SARS-CoV-2 variants have the capacity to infect the brain, via the olfactory pathway, regardless of clinical disease presentations. This means it is possible even mild infections can lead to the virus infiltrating the brain. “The next step will be to understand... whether the virus is able to persist in the brain beyond the acute [initial, short-term] phase of infection, and whether the presence of the virus can induce persistent inflammation and the symptoms described in cases of long COVID, such as anxiety, depression and brain fog” [brain damage].’ © 2023 Rich Haridy / New Atlas. ➲ Source © 2023 Institut Pasteur .
❦ Your brain is a vast city. The roads (myelin) in this city let cars move efficiently. Oligodendrocytes are the construction workers who maintain these roads. As we age, these workers slow down, causing traffic jams and slower thoughts. Enter SARS-CoV-2, the destructive rioter. It doesn’t just disrupt traffic; it damages the roads and chases away the construction crews. Weeks after the riot, the city still struggles to function, with long-lasting road damages and traffic jams. This is the ‘brain fog’ of post-COVID life. ❂ 📖 (24 Sep 2023 ~ Aging and Disease) Role of Microglia, Decreased Neurogenesis and Oligodendrocyte Depletion in Long COVID-Mediated Brain Impairments ➤ © 2023 Outbreak Updates ➲
❦ Your lungs are balloons made of the finest silk, allowing them to expand and contract effortlessly with each breath. SARS-CoV-2 is as a needle, puncturing and tearing this delicate fabric. In an attempt to heal, the body patches up the punctures, but instead of the original silk, it uses rough patches. These patches – scarring or fibrosis – make parts of the lung rigid, restricting its once flawless expansion. With each subsequent infection, more patches appear, further suffocating the lung’s true function. The virus doesn’t just infect. It sabotages the very essence of our breath. ❂ 📖 (6 Apr 2022 ~ Annals of Medicine and Surgery) Post COVID-19 pulmonary fibrosis; a meta-analysis study ➤ © 2023 Outbreak Updates ➲
❦ ‘The most common causes of acquired lymphocytopenia include: ➲ Protein-energy undernutrition. ➲ HIV infection. ➲ COVID-19 . ➲ Certain other viral infections. Patients with HIV infection routinely have lymphocytopenia, which arises from destruction of CD4+ T cells infected with the HIV virus. Patients with COVID-19 also frequently have lymphocytopenia ( 35% to 83% of patients ) . Lower lymphocyte counts portend a poor prognosis and an increased likelihood of requiring ICU admission and of dying from the disease. The cause of the lymphocytopenia is not completely understood, but COVID-19 can directly infect lymphocytes, and a cytokine-related apoptosis of the cells is likely. ➲ Lymphocytopenia is most often due to AIDS , and recently COVID-19 , or undernutrition, but it also may be inherited or caused by various infections, drugs, or autoimmune disorders. ➲ Patients have recurrent viral , bacterial , fungal , or parasitic infections .’ ❂ 📖 (Accessed 16 Sep 2023 ~ Merck & Co.) Entry for 'Lymphocytopenia' in Merck Manual ➤ © 2023 Merck & Co .
❦ ‘We have recently demonstrated a causal link between loss of gonadotropin-releasing hormone ( GnRH ), the master molecule regulating reproduction , and cognitive deficits during pathological aging , including Down syndrome and Alzheimer’s disease. Olfactory and cognitive alterations , which persist in some COVID-19 patients, and long-term hypotestosteronaemia in SARS-CoV-2-infected men are also reminiscent of the consequences of deficient GnRH, suggesting that GnRH system neuroinvasion could underlie certain post-COVID symptoms and thus lead to accelerated or exacerbated cognitive decline . We explored the hormonal profile of COVID-19 patients and targets of SARS-CoV-2 infection in post-mortem patient brains and human fetal tissue. We found that persistent hypotestosteronaemia in some men could indeed be of hypothalamic origin , favouring post-COVID cognitive or neurological symptoms , and that changes in testosterone levels and body weight over time were inversely correlated. Infection of olfactory sensory neurons and multifunctional hypothalamic glia called tanycytes highlighted at least two viable neuroinvasion routes . Furthermore, GnRH neurons themselves were dying in all patient brains studied , dramatically reducing GnRH expression. Human fetal olfactory and vomeronasal epithelia , from which GnRH neurons arise, and fetal GnRH neurons also appeared susceptible to infection . Putative GnRH neuron and tanycyte dysfunction following SARS-CoV-2 neuroinvasion could be responsible for serious reproductive , metabolic , and mental health consequences in long-COVID and lead to an increased risk of neurodevelopmental and neurodegenerative pathologies over time in all age groups .’ ❂ 📖 (12 Sep 2023 ~ eBioMedicine: Lancet Discovery Science) Long-COVID cognitive impairments and reproductive hormone deficits in men may stem from GnRH neuronal death ➤ © 2023 eBioMedicine: Lancet Discovery Science .
❦ — “I don’t know anyone with Long Covid.” — “Everyone I know is tired.” ❂ © 2023 Antiviral Marketing . ➲
❦ Children have largely been unaffected by severe COVID-19 compared to adults, but data suggest that they may have experienced new conditions after developing the disease. We compared 1656 exposed and 1656 unexposed children from 1 February 2020 to 30 November 2021. We found significantly higher risks for some new conditions in exposed children, including mental health issues and neurological problems . The overall excess risk for new-onset conditions after COVID-19 was 78% higher in the exposed than unexposed children. ❂ 📖 (9 Sep 2023 ~ Acta Paediatrica) Comparative study showed that children faced a 78% higher risk of new-onset conditions after they had COVID-19 ➤ © 2023 Di Chiara et al / Acta Paediatrica.
❦ ‘Individuals with SARS-CoV-2 infection can develop symptoms that persist well beyond the acute phase of COVID-19 or emerge after the acute phase, lasting for weeks or months after the initial acute illness. The post-acute sequelae of COVID-19 (PASC) , which include physical, cognitive, and mental health impairments, are known collectively as long COVID or post-COVID-19 condition (PCC) . The proportion of patients affected by post-COVID-19 condition might be in the range of 10–30% of those infected with SARS-CoV-2, although understanding of this condition is still evolving. Socio-economic factors are fundamental determinants of health after COVID-19. Individuals from low-income and middle-income countries, those from marginalised communities, and those who are socially disadvantaged are probably disproportionately affected. The post-COVID-19 condition is systemic, affecting various organ systems. PCC results in: an increased use of healthcare resources ; a decreased quality of life ; an increased susceptibility to subsequent viral or bacterial infection ; and leads to heightened vulnerability to perioperative morbidity and mortality for individuals who require a surgical procedure for any (unrelated) indication. With a large and growing global population of survivors of COVID-19, the impact on individuals, healthcare systems, communities, and society is likely to be substantial. At present, there are no specific treatments for post-COVID-19-condition.’ ❂ 📖 (17 July 2023 ~ The Lancet) Post-acute sequelae of COVID-19: understanding and addressing the burden of multisystem manifestations ➤ © 2023 Parotto et al / The Lancet.
❦ ‘Long COVID is the patient-coined term for the disease entity whereby persistent symptoms ensue in a significant proportion of those who have had COVID-19, whether asymptomatic, mild or severe. The disease burden spans from mild symptoms to profound disability, the scale making this a huge, new healthcare challenge. Long COVID will likely be stratified into several more or less discrete entities with potentially distinct pathogenic pathways. The evolving symptom list is extensive, multi-organ, multisystem and relapsing–remitting, including fatigue, breathlessness, neurocognitive effects and dysautonomia. A range of radiological abnormalities in the olfactory bulb, brain, heart, lung and other sites have been observed in individuals with Long COVID. Some body sites indicate the presence of microclots; these and other blood markers of hypercoagulation implicate a likely role of endothelial activation and clotting abnormalities. Diverse auto-antibody (AAB) specificities have been found, as yet without a clear consensus or correlation with symptom clusters. There is support for a role of persistent SARS-CoV-2 reservoirs and/or an effect of Epstein-Barr virus reactivation, and evidence from immune subset changes for broad immune perturbation. The oncoming burden of Long COVID faced by patients, healthcare providers, governments and economies is so large as to be unfathomable, which is possibly why minimal high-level planning is currently allocated to it.’ ❂ 📖 (11 July 2023 ~ Nature Reviews: Immunology) The immunology of long COVID ➤ © 2023 Altmann et al / Nature.
❦ From the start of this pandemic, UK healthcare workers have been risking their lives and health caring for Covid patients without adequate protection. A significant number are now disabled following preventable occupational exposure to SARS-CoV-2, and are being managed out of the door with no support system in place, and without means to financially support themselves and their families. Not only have they lost their health and independence; they have lost their careers and livelihoods, with many now facing financial destitution. One would think – given the circumstances under which we fell ill, and with current workforce shortages – that NHS employers would be eager to do everything to facilitate the return to work of healthcare workers with Long Covid. However, NHS employers are legally required to implement only ‘reasonable adjustments’ – and so things such as extended-phased-return, or adjustments to shift patterns, are not always being facilitated. Instead, an increasing number of employers are choosing to terminate contracts. We feel betrayed and completely abandoned. Infection control guidelines are fundamentally flawed: SARS-CoV-2 is airborne. It is outrageous that three-and-a-half years into this pandemic, staff and patients are still, knowingly and repeatedly, being exposed to a level-3 biohazard – a virus known to cause brain damage and significantly increased risk of life-threatening blood complications even in those recovered. Healthcare workers must be provided with respiratory protection and the air quality in hospitals be monitored and improved through the installation of ventilation systems and air filter units. © 2023 Dr. Kelly Fearnley . ➲ NHS Doctor, Chair & Co-Founder of Long Covid Doctors for Action (LCDA). ➲ ❂ 📖 (The Guardian ~ 6 Jul 2022) Who's clapping now? UK healthcare workers with Long Covid have been abandoned ➤ 📖 (PDF): (BMA ~ 4 July 2023) Over-exposed and under-protected: the long-term impact of COVID-19 on doctors ➤ 📖 Related: (BMJ ~ 29 Jan 2021) Up the line to death: Covid-19 has revealed a mortal betrayal of the world's healthcare workers ➤ 📖 Related: (Industrial Injuries Advisory Council ~ November 2022) Covid-19 and occupational impacts ➤
❦ Feeling validated that life is ‘back to normal’ as you see all of those unmasked people around you in restaurants, shops and cinemas? I’ll let you in on a little secret. Those who recognise the risk and who would be masked up aren’t even there. They are busy elsewhere staying healthy. More than 400 million now have Long Covid; a disease from Covid that can impact any organ system, and is proven to cause damage to the brain, heart, lung, kidney, gut, immune and multiple other systems. That’s one in 20 globally. How come you don’t know anyone with it? It’s one of three likely reasons… 1. They have been sick so long that they do what most chronically ill people do when they are asked, “How are you?” They say, “I’m fine”. 2. They don’t recognise the relation of their recent heart attack/memory impairment/new diabetes to their Covid illness in the last year. 3. It’s because they aren’t at that restaurant, movie, theatre, work night out as they don’t fancy worsening their already awful situation with a further infection. Out of sight, out of mind. Even those who know someone with Long Covid will minimise it, as it doesn’t fit with the general narrative that Covid is over. It’s too much cognitive dissonance for most people to handle. Easier to believe that everything’s OK, and it must “just be them being anxious”. It’s not over. I’ll let you in on another special secret; it’s not anxiety. It’s a calm determination to maintain health, in the full knowledge of what Covid can do. © 2023 NHS Palliative Care Medicine Consultant .
❦ I have seen a disproportionate number of young patients with advanced cancer over the last two years. They used to stand out: now it’s every week. The evidence points to direct Covid-driven mechanisms for rises in cancer risk. Will you hear about it in the news? Of course not. Covid’s over. It’s just anxiety now if you’re thinking about it. Except it’s not. It’ll take years for people to accept this. It’ll be too late. A number of my oncology colleagues have been commenting on how they’ve never seen such aggressively-progressive cancers in all their careers since Covid arrived. I’ve been seeing it as all these patients come to me. It isn’t normal. Alarm bells should be ringing loudly. The evidence: 📖 (22 Mar 2023 ~ Global Journal of Life Sciences and Biological Research) Cancer Related-Genes Enriched in Peripheral Blood Mononuclear Cells (PBMCs) of COVID-19 Patients: A Bioinformatics Study ➤ ‘SARS-CoV-2 can be considered a potential risk factor for increasing the probability of developing cancer.’ Study 1: 📖 (7 Jun 2022 ~ Frontiers in Oncology) SARS-CoV-2 M Protein Facilitates Malignant Transformation of Breast Cancer Cells ➤ ‘Coronavirus disease 2019 (COVID-19) has spread faster due to the emergence of SARS-CoV-2 variants, which carry an increased risk of infecting patients with comorbidities, such as breast cancer.’ Study 2: 📖 (9 Aug 2022 ~ Journal of Infection ) Is SARS-CoV-2 an oncogenic virus? ➤ ‘Gene expression of p53 [tumour suppressor] is downregulated in blood of COVID-19 patients. Downregulation persists at least 24 weeks after infection in long COVID-19 patients. Long-term reduction of p53 could have impact on carcinogenesis.’ 📖 (9 Aug 2022 ~ Journal of Infection) Letter to the editor: Is SARS-CoV-2 an oncogenic virus? ➤ Study 3: 📖 (22 Mar 2023 ~ Global Journal of Life Sciences and Biological Research) Cancer related-genes enriched in peripheral blood mononuclear cells (PBMCs) of COVID-19 patients. A bioinformatics study ➤ ‘Numerous cancer-related genes up-regulated in SARS-CoV-2-infected patients, particularly those genes participating in the cell-cycle regulation or engaged in cellular senescence processes.’ Study 4: 📖 (2 Jun 2023 ~ Biochimie) Possible cancer-causing capacity of COVID-19: Is SARS-CoV-2 an oncogenic agent? ➤ ‘One of the most worrying long-term effects of infection is the potential to induce malignant neoplasms, which will be a major health concern over the coming decades. SARS-CoV-2 infection affects many mechanisms that play a crucial role in cancer onset and progression including cell-cycle regulation, the RAAS system and inflammation / proliferation signaling pathways.’ ❂ Related reading : 📖 (9 Aug 2021 ~ Nature: Scientific Reports) More than 50 Long-term effects of COVID-19: a systematic review and meta-analysis ➤ 📖 (21 Jun 2021 ~ Nature: Scientific Reports) The risk of pancreatic adenocarcinoma following SARS-CoV family infection ➤ 📖 (4 Mar 2021 ~ Nature: Scientific Reports) COVID-19 engages clinical markers for the management of cancer and cancer-relevant regulators of cell proliferation, death, migration, and immune response ➤ 📖 (28 Jan 2021 ~ Nature: Scientific Reports) Meta-analysis of host transcriptional responses to SARS-CoV-2 infection reveals their manifestation in human tumors ➤ 📖 (25 Jan 2010 ~ Nature: Oncogene) Viral epigenome in human tumorigenesis ➤ 📖 (Dec 2006 ~ Yale Journal of Biology and Medicine) Viruses and human cancer ➤ ❂ © 2023 NHS Medical Consultant .
❦ Researchers at The University of Queensland have discovered viruses such as SARS-CoV-2 can cause brain cells to fuse, initiating malfunctions that lead to chronic neurological symptoms. SARS-CoV-2, the virus that causes COVID-19, has been detected in the brains of people with 'Long COVID' months after their initial infection. "We discovered COVID-19 causes neurons to undergo a cell fusion process, which has not been seen before," Professor Hilliard said. "After neuronal infection with SARS-CoV-2, the spike S protein becomes present in neurons, and once neurons fuse, they don't die." "They either start firing synchronously, or they stop functioning altogether." As an analogy, Professor Hilliard likened the role of neurons to that of wires connecting switches to the lights in a kitchen and a bathroom. "Once fusion takes place, each switch either turns on both the kitchen and bathroom lights at the same time, or neither of them," he said. "It's bad news for the two independent circuits." The discovery offers a potential explanation for persistent neurological effects after a viral infection. "In the current understanding of what happens when a virus enters the brain, there are two outcomes – either cell death or inflammation," Dr Martinez-Marmol said. "But we've shown a third possible outcome, which is neuronal fusion." Dr Martinez-Marmol said numerous viruses cause cell fusion in other tissues, but also infect the nervous system and could be causing the same problem there. "These viruses include HIV, rabies, Japanese encephalitis, measles, herpes simplex virus and Zika virus," he said. “Our research reveals a new mechanism for the neurological events that happen during a viral infection. “This is potentially a major cause of neurological diseases and clinical symptoms that is still unexplored.” ❂ 📖 (7 June 2023 ~ Science Advances) SARS-CoV-2 infection and viral fusogens cause neuronal and glial fusion that compromises neuronal activity ➤ 📖 (8 June 2023 ~ Queensland Brain Institute) COVID-19 can cause brain cells to 'fuse' ➤ © 2023 Martinez-Marmol & Hilliard / Queensland Brain Institute / University of Queensland.
❦ “What if Covid has been causing mass cognitive impairment and we are all living in an increasingly stupid society? Mad things could happen with that: imagine if hospitals got rid of masks or people started to believe Covid was just a cold? I know that’s far-fetched, but imagine!” ❂ © 2023 NHS Palliative Medicine Consultant .
❦ Prior to 2020, there were four endemic human coronaviruses – OC43, NL-63, 229E, and HKU1 – which were known to cause 10 to 15 percent of common colds – or the ‘Common Cold Coronaviruses’ (CCCs). From at least the 1970s, we’ve known that infection with these coronaviruses does not lead to lasting protection from reinfection – this is textbook knowledge. CCCs are not just colds – they can cause severe pneumonias, and exhibit a risk profile very similar to SARS-CoV-2 with age. If reinfection really did strengthen immunity against CCCs, then older people would be the least affected – because they would have been regularly infected with diverse variants of these viruses in their past. But that is not the case – and SARS-CoV-2 is not a CCC. SARS-CoV-2 has a wide array of accessory proteins that silence and disrupt our normal immune responses. As we get older, our immune systems start to lose their effectiveness – and we become more susceptible to disease. This process is called immunosenescence . Repeated exposure to a virus like SARS-CoV-2 is fast-tracking more people into immunosenescence at ever-earlier ages, with potentially serious repercussions for their health and longevity. SARS-CoV-2 is a particularly nasty virus that can also trigger the hyperactivation of our own immune systems to cause severe disease. Infection by SARS-CoV-2 has been shown to lead to an increase in autoantibodies and autoimmune disease. Approximately 25 percent of people who develop an autoimmune disease will experience multiple autoimmune syndrome, and will risk a cascade of autoimmune conditions. SARS-CoV-2, like its 2002 predecessor SARS-CoV-1, is both a respiratory and a systemic virus, with an extremely broad cell-type and tissue-tropism covering nearly the whole body. Its ability to infect and do damage to lungs, hearts, kidneys, cardiovascular systems and brains is particularly well-documented. If each subsequent infection results in additional internal organ and immune-system damage, then at some point the damage accumulated – together with the accelerated immune-system aging and normal aging processes – can reasonably be expected to outweigh the protective benefits of immunity developed from previous infections. SARS-CoV-2 reinfects more frequently than influenza or the common cold, infects a wider range of organs, does more damage and seems capable of persisting in a range of organs. So if SARS-CoV-2 behaves like a textbook virus – but does more damage more quickly and more regularly – at what point does the body reach its tipping point? ❂ There are two versions of this article: a 7-minute read in simplified language ; and the full editorial version complete with references, which is an 18-minute-read and aimed towards the medical and scientific communities . ❦ 7-minute primer ~ ‘SARS-CoV-2 and “Textbook” Immunity’ ➤ ❦ Full 18-minute editorial ~ ‘SARS-CoV-2 and “Textbook” Immunity’ ➤ ❂ 📖 (5 May 2023 ~ The John Snow Project) SARS-CoV-2 and "Textbook" Immunity ➤ © 2023 The John Snow Project.
❦ ‘Some viruses are known to be associated with the onset of specific cancers. These micro-organisms – oncogenic viruses or oncoviruses – can convert normal cells into cancer cells. Seven oncogenic viruses are known to promote tumorigenesis [tumour creation] in humans: Human papillomavirus (HPV) Hepatitis B and C viruses (HBV, HCV) Epstein-Barr virus (EBV) Human T-cell leukemia virus 1 (HTLV-1) Kaposi sarcoma-associated herpesvirus (KSHV) Merkel cell polyomavirus (MCPyV) Recent research indicates that SARS-CoV-2 infection and COVID-19 progression may predispose recovered patients to cancer onset and accelerate cancer development . This hypothesis is based on the growing evidence regarding the ability of SARS-CoV-2 to modulate oncogenic pathways, promoting chronic low-grade inflammation and causing tissue damage.’ ❂ 📖 (25 Apr 2023 ~ International Journal of Molecular Sciences) Deciphering the Relationship between SARS-CoV-2 and Cancer ➤ © 2023 Costanzo et al / International Journal of Molecular Sciences.
❦ Critically ill COVID-19 patients are highly susceptible to opportunistic fungal infection due to many factors, including virus-induced immune dysregulation , host-related comorbidities, overuse and misuse of antibiotics or corticosteroids, immune modulator drugs, and the emergencies caused by the pandemic. Fungal coinfection is a common complication of critically ill COVID-19 patients admitted to the ICU. Candidiasis , aspergillosis , and mucormycosis are the most common COVID-19-associated fungal infections and have a great impact on mortality rates . ❂ 📖 (18 Apr 2023 ~ BMC Infectious Diseases) Fungal infection profile in critically ill COVID-19 patients: a prospective study at a large teaching hospital in a middle-income country ➤ © 2023 Negm et al / BMC Infectious Diseases.
❦ The results presented here reveal that at least 85% [of the 214 patients with post COVID-19 syndrome] exhibit deficits in one neuropsychological test . Also, the youngest patients were those who showed the most marked and heterogeneous cognitive impairment , while the oldest patients maintained their cognitive functions preserved to a greater extent with only a mild impairment in attention and speed processing. ❂ 📖 (19 Apr 2023 ~ Nature: Scientific Reports) Cognitive impairment in young adults with post COVID-19 syndrome ➤ © 2023 Herrera et al / Nature.
❦ ‘COVID-19 patients have a hypercoagulability state, and thrombosis is a life-threatening complication of them.’ ✻ Hypercoagulability , also known as thrombophilia , is a condition in which there is an abnormally increased tendency towards blood clotting . ‘From the early days of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) outbreak to the present, clinical and basic studies have indicated that coronavirus disease 2019 (COVID-19) may be associated with coagulopathy ( CAC ), which is involved in its related morbidity and mortality. Deep vein thrombosis ( DVT ) and pulmonary embolism ( PE ) are common in COVID-19 patients and are remarkably high in the intensive care unit (ICU)–admitted patients. CAC can lead to the formation of circulating microthrombi and macrothrombi which can involve multiple sites, including the lungs , brain , heart , and visceral organs like kidneys and spleen . There is a close relationship between the immune system and coagulation. The components of the hemostatic system play a role in the body’s immunity, and the activation of the immune system strongly influences the hemostatic system. Abnormal activation of the immune system may promote the growth of pathologies associated with thrombosis. COVID-19 is accompanied by an immune-cell hyperactivation and excessive production of proinflammatory cytokines , known as “ cytokine storm ”. CAC is theorized to result from dysregulated interactions between the immune and coagulation systems .’ ❂ 📖 (19 Apr 2023 ~ Annals of Hematology) Status of major hemostatic components in the setting of COVID-19: the effect on endothelium, platelets, coagulation factors, fibrinolytic system, and complement ➤ © 2023 Annals of Hematology .
❦ 'The risk of herpes zoster (HZ) [ shingles ] remained significantly higher [ +60% ] in patients with COVID-19, compared with those without COVID-19. The higher risk of HZ in the COVID-19 cohort compared with that in the non-COVID-19 cohort remained consistent across subgroup analyses regardless of vaccine status, age, or sex. The risk of HZ within a 12-month follow-up period was significantly higher in patients who had recovered from COVID-19 compared with that in the control group.' ❂ 📖 (18 Apr 2023 ~ Journal of Medical Virology) Long-term risk of herpes zoster following COVID-19: A retrospective cohort study of 2 442 686 patients ➤ © 2023 Journal of Medical Virology.
❦ ‘Pulmonary arterial hypertension (PAH) is a pulmonary vascular disease characterized by the progressive elevation of pulmonary arterial pressures.’ Pulmonary Arterial Hypertension ( PAH ) is a progressive lung disease that affects the heart and lungs . It is caused when the tiny arteries in the lungs become thickened and narrowed , causing abnormally high blood pressure in the pulmonary artery . Symptoms include shortness of breath during exercise, fainting spells , dizziness , swelling of the ankles or legs , chest pain , and a racing pulse . ‘It is becoming increasingly apparent that inflammation contributes to the pathogenesis and progression of PAH. Several viruses are known to cause pulmonary arterial hypertension (PAH) , such as SARS-CoV-2 , Human Endogenous Retrovirus K (HERV-K), and Human Immunodeficiency Virus ( HIV ), in part due to acute and chronic inflammation .’ ❂ 📖 (18 Apr 2023 ~ International Journal of Molecular Sciences) Human Endogenous Retrovirus, SARS-CoV-2, and HIV Promote PAH via Inflammation and Growth Stimulation ➤ © 2023 International Journal of Molecular Sciences .
❦ The full picture of post-COVID-19 autoimmune diseases and their prevalence is lacking despite numerous case reports and small series. Two studies that use large cohorts now highlight that SARS-CoV-2 infection is linked to a substantially increased risk of developing a diverse spectrum of new-onset autoimmune diseases . The reports by Chang et al and Tesch et al provide a comprehensive overview of diverse new-onset autoimmune conditions after COVID-19. In addition, an earlier preprint of a retrospective matched cohort analysis using data from the Clinical Practice Research Datalink Aurum database of 458,147 SARS-CoV-2-infected and 1,818,929 uninfected adults across England between 31 January 2020 and 30 June 2021 reported that the incidence of type 1 diabetes mellitus , inflammatory bowel disease and psoriasis are significantly associated with SARS-CoV-2 infection. Some of the earliest evidence that SARS-CoV-2 infection leads to dysregulated immune responses came from paediatric patients who presented with multisystem inflammatory syndrome in children (MIS-C) , which, as the name indicates, involves diffuse organ system involvement and a clinical spectrum that overlaps with other hyperinflammatory syndromes , such as Kawasaki disease , toxic-shock syndrome , and macrophage activation syndrome . Since the start of the pandemic, many researchers have also reported isolated cases of adults with various post-COVID-19 autoimmune conditions. ❂ 📖 (12 Apr 2023 ~ Nature Reviews: Rheumatology) High risk of autoimmune diseases after COVID-19 ➤ © 2023 Sharma & Jagadeesh / Nature.
❦ The Linseman Laboratory is studying the long-term brain health effects of COVID-19 in individuals with and without traumatic brain injury (TBI). Preliminary data suggest that those with a history of both COVID-19 and TBI experience more severe Long COVID symptoms, a higher symptom burden , and more frequent symptoms . Those who reported having COVID-19 and TBI reported worse depressive symptoms , worse functional outcomes , and increased fatigue . ❂ 📖 (4 Apr 2023 ~ SciTechDaily) Researchers Discover Connection Between Traumatic Brain Injury and Long COVID ➤ © 2023 Linesman Laboratory / University of Denver / SciTechDaily.
‘We are entering a phase of long COVID and chronic disability.’ ❂ ❦ ‘As the numbers of hospitalizations and deaths are dropping, many individuals declare the pandemic all but over, comforted by the belief that infections are mild and less dangerous than the seasonal flu. However, the scientific literature these last few weeks has been filled with deeply concerning reports. We are entering a phase of long COVID and chronic disability. The number of COVID-19 cases in the United States is unknown since our case reporting system has become unreliable and substantially undercounts cases. In England, as of the week ending March 7, 2023, 1 in 40 people is positive for COVID-19 , and reinfections are frequently occurring. It is estimated that as of November 9, 2022, 94% of the U.S. population has been infected by SARS-CoV-2 , and 65% of the United States population has been infected multiple times . The odds of self-reported long COVID were 28% less after the second infection. Unfortunately, the damage of long COVID from a second infection adds to the first . One of the most concerning long-term effects of COVID-19 is immune dysfunction or hypofunction . Confirmatory research was reported this week, and summarized in a National Institute of Health news release which stated: ‘… findings suggest that SARS-CoV-2 infection damages the CD8⁺ T cell response , an effect akin to that observed in earlier studies showing long-term damage to the immune system after infection with viruses such as hepatitis C or HIV .’ The authors conclude that this dysfunction causes lasting damage and may ‘contribute to long COVID, perhaps rendering patients unable to respond robustly to subsequent infections by SARS-CoV-2 variants or other pathogens .’ * * 📖 (20 Mar 2023 ~ National Institutes for Health) SARS-CoV-2 infection weakens immune-cell response to vaccination ➤ These findings mirror those reported by Files et al who state: ‘Overall, expression of these activation and exhaustion markers indicated more severe immune dysregulation of CD8 ⁺ T cells in the hospitalized group.’ And they found that ‘ CD8⁺ T cell expression of exhaustion markers increased in non-hospitalized individuals over time ’. * * 📖 (4 Jan 2021 ~ Journal of Clinical Investigation) Sustained cellular immune dysregulation in individuals recovering from SARS-CoV-2 infection ➤ The authors’ finding of damage to the immune system “akin” to HIV is very concerning, as is the amplification of this result in the NIH news release. Infection Control Today previously reported that the probable cause of the surges in infections we are seeing is an immune dysfunction caused by COVID-19 . With minimal public health interventions, Sweden also experienced surges in respiratory syncytial virus (RSV) cases. Most recently, Sweden has undergone a significant surge in seasonal flu, with reports from the Public Health Agency of Sweden of unusually severe cases. These [Swedish influenza] cases have occurred in ‘... people under the age of 18 without underlying disease or condition, and have been very seriously ill with complications such as myocarditis or encephalitis.’ Other diseases are also rising , exemplified by reports of record-high severe Streptococcal infections and Candida auris . These spikes in infections caused by multiple pathogens are associated with the SARS-CoV-2 pandemic and the mounting evidence of post-COVID-19 immune dysfunction. Vaccinations can not only reduce the incidence of severe disease, but can also help to prevent long COVID, reducing the incidence by 30% to 40%. However, we have expressed concern regarding the bivalent booster’s effectiveness, and reported a rapid waning of booster-induced immunity in the elderly. [See Footnote.] Recently, researchers from the United States found that the relative bivalent booster effectiveness at 5 to 7 months in preventing hospitalizations relative to monovalent vaccine dosages (2, 3, or 4) was 42% and 59% compared to no vaccination. Using the third vaccine dose as a baseline, the UK Health Security Agency found that an additional (fourth) vaccine dosage had effectiveness against hospitalizations at 10 weeks of only 50% .’ Source: 📖 (21 Mar 2023 ~ Infection Control Today) COVID-19: Study Suggests Long-term Damage to Immune System ➤ ❂ Footnote: On waning vaccine effectiveness * ‘Vaccine effectiveness is an important point. Although much of the younger population received a get-out-of-hospital free card for the latest variant, senior citizens were in its crosshairs. During the last 6 months (since May of 2022), those over the age of 75 had a higher rate of hospitalizations than in the Delta surge; those between the ages of 65 and 75 had approximately the same. Both age groups continue to be at high risk for death and disability. However, data showed that for those 65 years of age and older, the monovalent vaccine’s (2 or more doses) effectiveness for preventing hospitalizations fell to 28% in less than a year. Results were worse for those individuals under 65 years – only 19%.’ * 📖 (24 Feb 2023 ~ Infection Control Today) How Soon Is Another Booster Needed? Durability of Vaccine-Induced Immunity ➤ ❂ © 2023 Infection Control Today . ➲
❦ The possible neurological consequences of SARS-CoV-2 infection, associated with physical and cognitive frailty, could lead to a worsening of Parkinson’s disease (PD) in infected patients or – more rarely – to an increase in the Parkinsonian symptomatology . Parkinson’s disease (PD) or Parkinsonism has been described after infections with viruses , such as the Epstein-Barr virus , hepatitis C virus , HIV , influenza A virus , Japanese encephalitis virus , varicella zoster virus , or West Nile virus . Therefore, the hypothesis that SARS-CoV-2 may have even longer-term effects on the brain and lead to an increase in cases of Parkinson’s disease, as occurred in the years following the Spanish flu , has been put forward. ❂ 📖 (23 Mar 2023 ~ Brain Science) Parkinson’s Disease, SARS-CoV-2, and Frailty: Is There a Vicious Cycle Related to Hypovitaminosis D? ➤ © 2023 Palermo et al / Brain Science.
❦ ‘Dr. Kashyap Patel (MD), CEO of Carolina Blood & Cancer Care Associates, sees something different in his practice since the onset of the COVID-19 pandemic – not just with cancer care, but with cancer itself. — “The trend is getting more and more alarming. We are noticing trends in hematological malignancies, breast cancer, colorectal carcinoma and pancreatic cancer.” With COVID-19 added to the mix, Patel now fears a “perfect storm” of factors will trigger inflammatory responses in some patients, causing cancer to arrive years earlier than normal and making it deadlier once it is diagnosed.’ ❂ 📖 (22 Mar 2023 ~ Evidence-Based Oncology) Kashyap Patel, MD, Sees Link Between COVID-19 and Cancer Progression, Calls for More Biomarker Testing ➤ © 2023 Hayden Klein / Evidence-Based Oncology.
‘ We are drunk-driving in healthcare... with a pathogen that has a 10% fatality rate in that setting. ’
‘ Vaccine effectiveness against SARS-CoV-2 [COVID-19] infection declines markedly with time and Omicron variants . ’
‘ While acute [short-term] symptoms of reinfection are generally milder, the severity and incidence rate of long COVID increase significantly with the number of reinfections . ’
‘ These findings have important implications for understanding the potential impact of COVID-19 on long-term immune function and susceptibility to pathogens . ’
‘ For patients already battling Alzheimer’s disease , studies indicate that Covid can exacerbate brain inflammation , damage immune cells , and accelerate the disease . Even previously healthy older adults face an increased risk of cognitive impairment and new-onset dementia after infection. Mild Covid cases in younger adults have also been linked to brain issues affecting memory and thinking . ’
‘But even people who had not been hospitalized had increased risks of many conditions, ranging from an 8% increase in the rate of heart attacks to a 247% increase in the rate of heart inflammation.’ Nature (2 Aug 2022) ‘Either symptomatic or asymptomatic SARS-CoV-2 infection is associated with increased risk of late cardiovascular outcomes and has causal effect on all-cause mortality in a late post-COVID-19 period.’ The American Journal of Cardiology (15 Sep 2023)
‘The proportions of PACS [PASC/Long Covid] patients experiencing chest pain, palpitation, and hypertension as sequelae were 22% , 18% , and 19% respectively.’
‘Before Omicron, natural infection provided strong and durable protection against reinfection, with minimal waning over time. However, during the Omicron era, protection was robust only for those recently infected, declining rapidly over time and diminishing within a year.’
‘Scientists discover that even mild COVID-19 can alter brain proteins linked to Alzheimer’s disease, potentially increasing dementia risk. COVID-19-positive individuals exhibited lower cognitive test performance compared to controls – equivalent to almost two years of age-related cognitive decline. ’
‘The predominant symptoms , often clustering together, remain fatigue , cognitive disturbance and chest symptoms , including breathlessness , with sleep disorder and anxiety as additional complaints. Many patients with persistent PCS show impaired executive functioning , reduced cognitive processing speed and reduced physical exercise capacity .’
❦ On that 700-day cough... It’s a new thing, but it’s only reserved for inside supermarkets and offices. And pharmacies and hospitals and care homes. Oh, and your living-room. But apart from that, it’s not exactly a deal-breaker. I mean, c’mon. They put up with way worse in the 1900s. © 2024 C19.Life ❂
❦ “If you are letting yourself get infected and taking no precautions against passing it on, you are not a passive bystander for your next infection. You’ve participated in creating it.”
❦ ‘In this population of healthy young adult US Marines with mostly either asymptomatic or mild acute COVID-19, one fourth reported physical , cognitive , or psychiatric long-term sequelae of infection. The Marines affected with PASC [Post-Acute Sequelae of COVID-19 / Post-COVID-19 Complications / ‘Long Covid’] showed evidence of long-term decrease in functional performance suggesting that SARS-CoV-2 infection may negatively affect health for a significant proportion of young adults .’ ❂ ‘Among the 899 participants, 88.8% had a SARS-CoV-2 infection. Almost a quarter (24.7%) of these individuals had at least one COVID-19 symptom that lasted for at least 4 weeks meeting the a priori definition of PASC established for this study. Among those with PASC, 10 had no acute SARS-CoV-2 symptoms after PCR-confirmed infection suggesting that PASC can occur among asymptomatic individuals. Many participants reported that lingering symptoms impaired their productivity at work, caused them to miss work, and/or limited their ability to perform normal duty/activities. Marines with PASC had significantly decreased physical fitness test scores up to approximately one year post-infection with a three-mile run time that averaged in the 65th percentile of the reference cohort. [ PASC was associated with a significantly increased 3-mile run time on the standard Marine fitness test. PASC participants ran 25.1 seconds slower than a pre-pandemic reference cohort composed of 22,612 Marine recruits from 2016 to 2019. A three-mile run evaluates aerobic exercise , overhead lifting of an ammunition can and pull-ups evaluate strength , and shooting a rifle evaluates fine-motor skills .] Scores for events evaluating upper body (pull-ups, crunches, and ammo-can lift) were not significantly reduced by PASC; however, overall physical fitness scores were reduced. ‘The poorer run times and overall scores among PASC participants are indicative of on-going functional effects.’ Standardized health-based assessments for somatization, depression, and anxiety further highlighted the detrimental health effects of PASC. Almost 10% of participants with PASC had PHQ-8 scores ≥10. Increased somatization * has been associated with increased stress, depression, and problems with emotions. * [ Somatization / Somatisation = Medical symptoms caused by psychological stress.] Additionally, PASC participants had higher GAD-7 scores suggesting increased anxiety in a population with unique inherent occupational stressors associated with higher rates of anxiety, depression, and post-traumatic stress disorder. ‘Increased severity of anxiety among those with PASC, combined with greater rates of mental health disorders in general, could portend an ominous combination and should be closely followed.’ Like others, we identified cardiopulmonary symptoms as some of the most prevalent. The high prevalence of symptoms like shortness of breath, difficulty breathing, cough, and fatigue is particularly notable when combined with decreased objective measures of aerobic performance such as running. These results suggest pathology in the cardiopulmonary system. In contrast we observed no reduction in scores assessing strength and marksmanship suggesting the lack of detectable pathology in the neuro-musculoskeletal system. We have previously found in this same cohort that SARS-CoV-2 infection causes prolonged dysregulation of immune cell epigenetic patterns like auto-immune diseases. Based on the reported PASC symptoms, the potential current and future public health implications in this population could be substantial. ‘Chronic health complications from PASC, especially in a young and previously healthy population with a long life expectancy, could decrease work productivity and increase healthcare costs.’ Significant changes in the Years-of-Life lived with a disability can disproportionally increase disability-adjusted life-years, and should be considered when allocating resources and designing policy.’ ❂ 📖 (23 Oct 2024 ~ The Lancet: Regional Health/America) Clinical and functional assessment of SARS-CoV-2 sequelae among young marines – a panel study ➤ © 2024 The Lancet .
❦ If parents, and politicians and teachers, and healthcare workers and public health bodies wanted things to change, all they need do is read . It’s all there. But they don’t. They won’t. And they insist on their medical and scientific flat-earthing – hand-sanitiser for aerosol-transmitted disease – because they prefer the world to be flat. So let them walk off the edge of the world. [ Caveat: The earth is not flat, and doing nothing will not flatten the curve – but walk far enough, and you are likely to fall off a cliff.] © 2024 C19.Life ❂
❦ NHS nurse: — “Shit, I just got a needlestick injury.” ❦ 2024: — “Yeah, well, whatever. We all gotta die of something.” ❂ © 2024 C19.Life .
‘In those school-rooms where ventilation is imperfect and the air impure, six sevenths of the money expended to educate a child is wasted.’ ❂ The Ventilation and Warming of School Buildings (1887) By Gilbert B. Morrison Published by D. Appleton and Company, New York. 1887. Accessed 10 Apr 2024 Preface (p.xxii) ❦ ‘I am fully convinced that people are prematurely dying by thousands simply from a lack of correct and positive convictions concerning impure air; for, when the true nature of a danger is fully appreciated, the requisite means to avert it will generally be found.’ ❂ Chapter II: The Effects Of Breathing Impure Air (pp.20-23) ❦ ‘Impure air is also believed by the best authorities to be one of the principal causes of epidemics. Dr. Carpenter, than whom there is no abler authority, says: “It is impossible for anyone who carefully examines the evidence to hesitate for a moment in the conclusion that the fatality of epidemics is almost invariably in precise proportion to the degree in which an impure atmosphere has been habitually respired.” The Board of Health of New York conclude that forty per cent of all deaths are caused by breathing impure air. In view of such alarming facts, this same board declares: “Viewing the causes of preventable diseases, and their fatal results, we unhesitatingly state that the first sanitary want in New York and Brooklyn is ventilation .” Direct experiment proves that the air in our school-rooms is impure in almost all cases, and in a majority of them to a degree far beyond the danger line. In view of these facts, and the results as proved by the authorities above cited, why is it regarded by the public with such indifference? When a school-house is blown down by a hurricane, killing and maiming a score of children, it is justly regarded as a great calamity; a vacation is given to quiet the excited fears of parents and children; investigating committees are appointed to locate the responsibility, and the faces of the whole populace are blanched with apprehension. Why is this? Why does the intelligent parent send his child to a school-room poorly ventilated and crowded with children, some of whom are breathing into a stagnant air the germs of disease and death, while others, from unwashed bodies, are delivering into it their deadly emanations, and all without a protest on the part of those even who provide proper hygienic conditions at home? It is because the effects of the one are immediate, occupy little time, the number killed can be actually counted, and the exact magnitude of the calamity estimated all at once. In the other case the process is slower, but of far greater extent; the actual results are by the general public less definitely known, and custom and attention to other matters divert the attention, and the deadly destruction of the innocents by impure air goes on silently, constantly, and powerfully. While noisy demonstrations like that of the cyclone attract attention, and inspire fear and terror, it is in the silent forces that the danger lies. Nature’s most destructive forces, as well as her strongest constructive ones, are silent in their operations; but when Science detects a silent, insidious enemy to human welfare, it is not only our duty to assume an attitude of self-defense and self-protection, but it should be regarded as folly not to do so.’ ❦ On high CO₂ levels connected to poor performance in schools: ‘The effects of breathing impure air thus far considered are pathological, but it has its pedagogical and economical aspects. Every observing teacher knows the immediate relation between the vitiated air in the school-room and the work he wishes the pupils to perform. Much of the disappointment of poor lessons and the tendency to disorder are due directly to this cause. The brain unsupplied with a proper amount of pure blood [oxygen] refuses to act, and the will is powerless to arouse the flagging energies; the general feeling of discomfort, dissatisfaction, and unrest which always accompanies a bad state of the blood. From an economical standpoint it would, of course, be impossible to estimate the financial waste of breathing impure air, but it can not but be enormous. In any discussion of the feasibility of incurring the additional expense of the most perfect ventilation, this loss occasioned by the want of such ventilation must not be ignored.’ ❂ Chapter III: The Air (pp.25-26) ❦ On ventilation, air filtration, and the super-spreading of diverse diseases in classrooms: ‘Wherever an unusual amount of unwholesome matter is being evolved, there especially should the purifying conditions be present; air in such places, to remain pure, must be changed in rapid succession, in order that dilution, diffusion, and oxidation may fulfill their legitimate functions. In a school-room the contaminating process can not but be rapid, and wherever ample provision is not made for rapidly changing the air of the room a dangerous condition of affairs is sure to exist. Bacteria of many forms, and spores of fungi, are also found in the air, and all these organisms are known to thrive in the organic impurities found in the air.’ ❂ Chapter IV: Examination Of The Air (p.33) ❦ On measuring CO₂ levels as a proxy to establishing content of (infectious) re-breathed air: ‘A complete analysis of impure air comprehends the quantitative and qualitative tests for carbonic [sic] dioxide, free ammonia, and other nitrogenous matter, oxidizable matters, nitrous and nitric acids, and hydrogen sulphide; but for ordinary practical purposes the determination of the CO₂ is by far the most important, and is ordinarily the only one which need be made. While the poisonous qualities of the air are not wholly due to the presence of the CO₂ per se, the amount of this gas found to be present is, in air made impure by respiration, generally a good measure for other impurities to which the poisonous quality is principally due. Owing to this fact, a careful test for the amount of CO₂ contained in a given atmosphere is generally the only one which need be made where air is tested merely to determine its respiratory purity.’ ❂ 📖 (Accessed 10 Apr 2024 ~ D. Appleton & Company / Google Books) The Ventilation and Warming of School Buildings ➤ ❂ My thanks to Maarten De Cock for alerting me to this gem of a book. ➲
❦ SARS-CoV-2 – the virus that causes Covid-19 – is airborne . In May 2021, the WHO officially recognised that SARS-CoV-2 is airborne via microscopic aerosols – meaning that the virus is transmissible through the air at both long and short range .
‘ Reinfection , which is now the dominant type of SARS-CoV-2 infection , is not inconsequential ; it can trigger de novo Long Covid or exacerbate its severity . Each reinfection contributes additional risk of Long Covid: cumulatively , two infections yield a higher risk of Long Covid than one infection , and three infections yield a higher risk than two infections .’
❦ This study confirms everything that I have seen in the microscope over the last few years. The authors of the study use a technique called dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI), an imaging technique that can measure the density, integrity, and leakiness of tissue vasculature. Comparing all individuals with previous COVID infection to unaffected controls revealed decreased general brain volume in patients with brain fog along with significantly reduced cerebral white matter volume in both hemispheres in the recovered and brain fog cohorts . Covid-19 induces brain volume loss and leaky blood-brain barrier in some patients. How can this be more clear? © 2024 Danielle Beckman. ➲ ❂ 📖 (22 Feb 2024 ~ Nature: Neuroscience) Blood–brain barrier disruption and sustained systemic inflammation in individuals with long COVID-associated cognitive impairment ➤ 📖 (22 Feb 2024 ~ Nature: Neuroscience) Leaky blood–brain barrier in long-COVID-associated brain fog ➤ ➲ Layperson overview: 📖 (February 2024 ~ Genetic Engineering and Biotechnology News) Leaky Blood Vessels in the Brain Linked to Brain Fog in Long COVID Patients ➤ Related: 📖 (7 Feb 2022 ~ Nature: Cardiovascular Research) Blood–brain barrier link to human cognitive impairment and Alzheimer’s disease ➤ ❂ © 2024 Nature .
‘The very first canon of nursing... the first essential to the patient... is this: to keep the air he breathes as pure as the external air, without chilling him .’ ❂ Notes on Nursing (1860 edition) By Florence Nightingale First Published 1859. Revised edition reprinted in 1860 by Harrison of Pall Mall Accessed 19 Feb 2024 ❦ Chapter I – Ventilation and Warming ‘The very first canon of nursing, the first and the last thing upon which a nurse’s attention must be fixed, the first essential to the patient, without which all the rest you can do for him is as nothing, with which I had almost said you may leave all the rest alone, is this: TO KEEP THE AIR HE BREATHES AS PURE AS THE EXTERNAL AIR, WITHOUT CHILLING HIM. Yet what is so little attended to? Even where it is thought of at all, the most extraordinary misconceptions reign about it. Even in admitting air into the patient’s room or ward, few people ever think where that air comes from. It may come from a corridor into which other wards are ventilated, from a hall, always unaired, always full of the fumes of gas, dinner, of various kinds of mustiness; from an underground kitchen, sink, wash-house, water-closet, or even, as I myself have had sorrowful experience, from open sewers loaded with filth; and with this the patient’s room or ward is aired, as it is called – poisoned, it should rather be said. Always air from the air without, and that, too, through those windows, through which the air comes freshest. From a closed court, especially if the wind do not blow that way, air may come as stagnant as any from a hall or corridor. I know an intelligent humane house surgeon who makes a practice of keeping the ward windows open. The physicians and surgeons invariably close them while going their rounds; and the house surgeon, very properly, as invariably opens them whenever the doctors have turned their backs. I have known a medical officer keep his ward windows hermetically closed, thus exposing the sick to all the dangers of an infected atmosphere, because he was afraid that, by admitting fresh air, the temperature of the ward would be too much lowered. This is a destructive fallacy. To attempt to keep a ward warm at the expense of making the sick repeatedly breathe their own hot, humid, putrescing atmosphere is a certain way to delay recovery or to destroy life.’ ❂ ‘I have known cases of hospital pyæmia quite as severe in handsome private houses as in any of the worst hospitals, and from the same cause, viz., foul air. Yet nobody learnt the lesson. Nobody learnt anything at all from it.’ ❂ ✪ C-19: On schools ‘Of all places, public or private schools, where a number of children or young persons sleep in the same dormitory * , require this test of freshness to be constantly applied.’ * [ C-19 Note: You might substitute ‘sleep’ and ‘dormitory’ with ‘study’ and ‘classroom’ in this section.] ‘If it be hazardous for two children to sleep together in an unventilated bedroom, it is more than doubly so to have four, and much more than trebly so to have six under the same circumstances. People rarely remember this; yet, if parents were as solicitous about the air of school bedrooms as they are about the food the children are to eat, and the kind of education they are to receive, at school, depend upon it due attention would be bestowed on this vitally important matter, and they would cease to have their children sent home either ill, or because scarlet fever or some other “current contagion” had broken out in the school. There are schools where attention is paid to these things, and where “children’s epidemics” are unknown.’ ❂ ✪ C-19: Offices, shops, factories, and other workplaces ‘How much sickness, death, and misery are produced by the present state of many factories, warehouses, workshops, and workrooms!’ ‘How much sickness, death, and misery are produced by the present state of many factories, warehouses, workshops, and workrooms! The places where poor dressmakers, tailors, letter-press printers, and other similar trades have to work for their living, are generally in a worse sanitary condition than any other portion of our worst towns. Many of these places of work were never constructed for such an object. They are badly adapted garrets, sitting-rooms, or bedrooms, generally of an inferior class of house. No attention is paid to cubic space or ventilation. The poor workers are crowded on the floor to a greater extent than occurs with any other kind of over-crowding. The constant breathing of foul air, saturated with moisture, and the action of such air upon the skin renders the inmates peculiarly susceptible of the impression of cold, which is an index indeed of the danger of pulmonary disease to which they are exposed. The result is, that they make bad worse, by over-heating the air and closing up every cranny through which ventilation could be obtained. In such places, and under such circumstances of constrained posture, want of exercise, hurried and insufficient meals, long exhausting labour and foul air – is it wonderful that a great majority of them die early of chest disease, generally of consumption? Intemperance is a common evil of these workshops. The men can only complete their work under the influence of stimulants, which help to undermine their health and destroy their morals, while hurrying them to premature graves. Employers rarely consider these things. Healthy workrooms are no part of the bond into which they enter with their work-people. They pay their money, which they reckon their part of the bargain. And for this wage the workman or workwoman has to give work, health, and life. Do men and women who employ fashionable tailors and milliners ever think of these things? And yet the master is no gainer. His goods are spoiled by foul air and gas fumes, his own health and that of his family suffers, and his work is not so well done as it would be, were his people in health. And the time will come when it will be found cheaper to supply shops, warehouses, and work-rooms with pure air than with foul air.’ ‘And the time will come when it will be found cheaper to supply shops, warehouses, and work-rooms with pure air than with foul air.’ ❂ ✪ C-19: On ‘air-tests’, and measuring CO₂ as a proxy for estimating prevalence of airborne disease indoors ‘Dr. Angus Smith’s air-test, if it could be made of simple application, would be invaluable to use in every sleeping and sick room. Just as without the use of a thermometer no nurse should ever put a patient into a bath, so, if this air-test were made in some equally simple form, should no nurse, or mother, or superintendent, be without it in any ward, nursery, or sleeping-room. But to be used, the air-test must be made as simple a little instrument as the thermometer, and both should be self-registering. ‘...the air-test must be made as simple a little instrument as the thermometer, and both should be self-registering.’ The senses of nurses and mothers become so dulled to foul air that they are perfectly unconscious of what an atmosphere they have let their children, patients, or charges sleep in. But if the tell-tale air-test were to exhibit in the morning, both to nurses and patient and to the superior officer going round, what the atmosphere has been during the night, I question if any greater security could be afforded against a recurrence of the misdemeanour.’ ❂ ✪ C-19: ... And back to the school-room, testing its air, and combatting airborne pathogens ‘And, oh! the crowded national school! where so many children’s epidemics have their origin; and the crowded, unventilated work-room, which sends so many consumptive men and women to the grave; what a tale its air-test would tell! We should have parents saying, and saying rightly, “I will not send my child to that school. I will not trust my son or my daughter in that tailor’s or milliner’s workshop, the air-test stands at ‘Horrid.’” ‘We should have parents saying, and saying rightly, “I will not send my child to that school... the air-test stands at Horrid .”’ And the dormitories of our great boarding schools! Scarlet fever would be no more ascribed to contagion but to its right cause, the air-test standing at “Foul.” We should hear no longer of “mysterious dispensations,” nor of “plague and pestilence” being “in God’s hands,” when, so far as we know, He has put them into our own. The little air-test would both betray the cause of these “mysterious pestilences,” and call upon us to remedy it.’ ❂ ❦ Chapter II – Health of Houses ‘There are five essential points in securing the health of houses:– Pure air. Pure water. Efficient drainage. Cleanliness. Light. Without these, no house can be healthy. And it will be unhealthy just in proportion as they are deficient. To have pure air, your house must be so constructed as that the outer atmosphere shall find its way with ease to every corner of it. ‘To have pure air, your house must be so constructed as that the outer atmosphere shall find its way with ease to every corner of it.’ House architects hardly ever consider this. The object in building a house is to obtain the largest interest for the money, not to save doctor’s bills to the tenants. But, if tenants should ever become so wise as to refuse to occupy unhealthily constructed houses, and if Insurance Companies should ever come to understand their interest so thoroughly as to pay a Sanitary Surveyor to look after the houses where their clients live, speculative architects would speedily be brought to their senses. As it is, they build what pays best. And there are always people foolish enough to take the houses they build. And if in the course of time the families die off, as is so often the case, nobody ever thinks of blaming any but Providence for the result. Ill-informed medical men aid in sustaining the delusion, by laying the blame on “current contagions”. Badly constructed houses do for the healthy what badly constructed hospitals do for the sick.’ ‘Badly constructed houses do for the healthy what badly constructed hospitals do for the sick.’ ❂ ❦ Conclusion ‘The whole of the preceding remarks apply even more to children and to puerperal women than to patients in general. They also apply to the nursing of surgical, quite as much as to that of medical cases. Indeed, if it be possible, cases of external injury require such care even more than sick. In surgical wards, one duty of every nurse certainly is prevention. Fever, or hospital gangrene, or pyæmia, or purulent discharge of some kind may else supervene. If she allows her ward to become filled with the peculiar close fœtid smell, so apt to be produced among surgical cases, especially where there is great suppuration and discharge, she may see a vigorous patient in the prime of life gradually sink and die where, according to all human probability, he ought to have recovered. The surgical nurse must be ever on the watch, ever on her guard, against want of cleanliness, foul air, want of light, and of warmth.’ ‘In surgical wards, one duty of every nurse certainly is prevention.’ ❂ 📖 (Accessed 19 Feb 2024 ~ Original text copied from FiftyWordsForSnow.com) Notes on Nursing (1860) ➤ 📖 (Accessed 19 Feb 2024 ~ Original scanned pages from Google Books) Notes on Nursing (1860) ➤ ❂
❦ LitCovid is the most comprehensive online resource on SARS-CoV-2 / COVID-19, providing access to 417,800+ relevant articles on PubMed. The library of scientific articles is updated daily, and categorised by different research topics (e.g. transmission), as well as geographic locations. ➲ Date accessed: 18 Feb 2024 . ❂ ❦ Useful Categories ✪ Transmission ➤ Characteristics and modes of SARS-CoV-2 transmission. ✪ Prevention ➤ Prevention, control, response and management strategies. ✪ Long Covid ➤ Post-COVID-19 Conditions/Complications (PCC) / Post-Acute Sequelae of COVID-19 (PASC). ✪ Case Reports ➤ Descriptions of specific patient cases. ✪ Treatments ➤ Treatment strategies, therapeutic procedures, and vaccine development. ✪ Forecasting ➤ Modelling, and estimating the trend of SARS-CoV-2 spread. ❂ ➲ LitCovid Online Library ➤ © 2024 National Institutes for Health (NIH) / National Center for Biotechnology Information (NCBI) / U.S. National Library of Medicine (NLM USA).
❦ Mitigation = ‘Lessening the force or intensity of something unpleasant; the act of making a condition or consequence less severe.’ 1. Clean indoor air . The priority should be air filters in schools and hospitals . New ventilation and air filtration standards for all public spaces . Grants made available to businesses to upgrade ventilation and air filtration . 2. FFP2/3 [N95/N99] respirators (masks) in all healthcare settings . 3. Free Covid vaccines available to everyone. 4. Wider access to Covid anti-viral treatments . 5. Free LFT/PCR testing . 6. Improved Covid surveillance , including wastewater monitoring and Long Covid prevalence . 7. Paid sick-leave , so that people don’t go to work when ill. 8. Respirators (masks) on public transport , including flights . 9. Better support and treatments for Long Covid patients . ... and last, but by no means least: 10. A public education campaign on the long-term risks of Covid – and why people should do more to protect themselves. ❦ Addendum : Allocate adequate research funding for a sterilising vaccine as well as treatments/cure for Long Covid . ❂ © 2024 Cat in the Hat . ➲
❦ ‘The occurrences of respiratory disorders among patients who survived for 30 days after the COVID-19 diagnosis continued to rise consistently, including asthma , bronchiectasis , COPD , ILD , PVD * , and lung cancer . * COPD = Chronic obstructive pulmonary disease . ILD = Interstitial lung disease . PVD = Peripheral vascular disease . With the severity of the acute phase of COVID-19, the risk of all respiratory diseases increases progressively. Besides, during the 24-months follow-up, we observed an increasing trend in the risks of asthma and bronchiectasis over time, which indicates that long-term monitoring and meticulous follow-up of these patients is essential. These findings contribute to a more complete understanding of the impact of COVID-19 on the respiratory system and highlight the importance of prevention and early intervention of these respiratory sequelae of COVID-19. In this study, several key findings have been further identified. Firstly, our research demonstrates a significant association between COVID-19 and an increased long-term risk of developing various respiratory diseases. Secondly, we found that the risk of respiratory disease increases with severity in patients with COVID-19, indicating that it is necessary to pay attention to respiratory COVID-19 sequelae in patients, especially those hospitalized during the acute stage of infection. This is consistent with the findings of Lam et al., who found that the risk of some respiratory diseases (including chronic pulmonary disease, acute respiratory distress syndrome and ILD) increased with the severity of COVID-19. Notably, however, our study found that asthma and COPD remained evident even in the non-hospitalized population. This emphasizes that even in cases of mild COVID-19, the healthcare system should remain vigilant. Thirdly, we investigated differences in risk across time periods, as well as the long-term effects of COVID-19 on respiratory disease. During the 2-years follow-up period, the risks of COPD, ILD, PVD and lung cancer decreased, while risks of asthma and bronchiectasis increased. Fourthly, our study showed a significant increase of the long-term risk of developing asthma, COPD, ILD, and lung cancer diseases among individuals who suffered SARS-CoV-2 reinfection. This finding emphasizes the importance of preventing reinfection of COVID-19 in order to protect public health and reduce the potential burden of SARS-CoV-2 reinfection. Interestingly, vaccination appears to have a potentially worsening effect on asthma morbidity compared with other outcomes. This observation aligns with some previous studies that have suggested a possible induction of asthma onset or exacerbation by COVID-19 vaccination. It suggests that more care may be necessary for patients with asthma on taking the COVID vaccines. The underlying mechanisms associated with COVID and respiratory outcomes are not fully understood, but several hypotheses have been proposed. First, SARS-CoV-2 can persist in tissues (including the respiratory tract), as well as the circulating system for an extended period of time after the initial infection. This prolonged presence of the virus could directly contribute to long-term damage of the respiratory tissues, consequently leading to the development of various respiratory diseases. Second, it has been observed that SARS-CoV-2 infection can lead to prolonged immunological dysfunctions, including highly activated innate immune cells, a deficiency in naive T and B cells, and increased expression of interferons and other pro-inflammatory cytokines. These immune system abnormalities are closely associated with common chronic respiratory diseases – asthma, bronchiectasis, COPD, as well as the development of lung cancer. Next, SARS-CoV-2 itself has been shown to drive cross-reactive antibody responses, and a range of autoantibodies were found in patients with COVID-19. In conclusion, our research adds to the existing knowledge regarding the effects of COVID-19 on the respiratory system. Specifically, it shows that the risk of respiratory illness increases with the severity of infection and reinfection. Our findings emphasize the importance of providing extended care and attention to patients previously infected with SARS-CoV-2.’ ❂ 📖 (17 Feb 2024 ~ The Lancet: eClinical Medicine) Long-term risks of respiratory diseases in patients infected with SARS-CoV-2: a longitudinal, population-based cohort study ➤ © 2024 The Lancet: eClinical Medicine .
❦ Chronic disease is like the perfect medical crime. The cause is usually long gone by the time the disease manifests, and nobody links the two until it’s much too late for most. ❂ © 2024 Henry Madison . ➲
❦ It’s really not in the interest of the virus to kill us quickly. That’s why it has mutated to immune escape. That way it enters silently, and then eats you slowly whilst you’re still a spreading vector. Refrigerator trucks are long gone. That’s all the political class wanted. The unseen costs of CVD [cardiovascular disease] , DM [diabetes mellitus] , and both dementia and Parkinson’s Disease are the train coming down the tunnel. The economists are catching up. The actuaries are already there. Politicians and most people? Not yet... ❂ © 2024 Dr. David Joffe, PhD, FRACP / Respiratory Physician ➲ .
❦ “I was in hospital for tests this morning. A nurse asked me: — “How come so many people are wearing masks? Is there something I don’t know?” I almost lost the power of speech.” ❂ © 2024 George Monbiot . ➲
❦ Genomic epidemiology of SARS-CoV-2 with subsampling focused globally since pandemic start. ➲ Built with nextstrain/ncov . Maintained by the Nextstrain team . Enabled by data from GISAID . ➲ Data updated: 21 Jan 2024. ➲ Date accessed: 21 Jan 2024. ❂ © 2024 NextStrain.org ➲
❦ “Every single case in which a person with COVID-19 infects another person in a healthcare setting – patient, relative, or hospital staff member – is a significant failure of hospital procedures. Every single instance .” ❂ © 2024 Professor Steve Robson MPH MD PhD ~ President, Australian Medical Association (AMA) . ➲
❦ Mike Honey’s Variant Visualiser (COVID-19 Genomic Sequence Analysis). The region of ‘Oceania/Australia’ is set by default, as the visualiser was created by Mike Honey , a Data Visualisation and Data Integration specialist in Melbourne, Australia. ➲ Choose your country by clicking on the ‘ Continent, Country, Location ’ dropdown menu in the top-right-hand corner . The variant visualiser is free to use, and is automatically updated every time you open the link. ❂ © 2024 Mike Honey .
❦ ‘Although some studies have shown neuroimaging and neuropsychological alterations in post-COVID-19 patients, fewer combined neuroimaging and neuropsychology evaluations of individuals who presented a mild acute infection. Here we investigated cognitive dysfunction and brain changes in a group of mildly infected individuals. We conducted a cross-sectional study of 97 consecutive subjects ( median age of 41 years ) without current or history of psychiatric symptoms (including anxiety and depression) after a mild infection , with a median of 79 days (and mean of 97 days ) after diagnosis of COVID-19. We performed semi-structured interviews, neurological examinations, 3T-MRI scans, and neuropsychological assessments. The patients reported memory loss ( 36% ), fatigue ( 31% ) and headache ( 29% ). The quantitative analyses confirmed symptoms of fatigue ( 83% of participants), excessive somnolence ( 35% ), impaired phonemic verbal fluency ( 21% ), impaired verbal categorical fluency ( 13% ) and impaired logical memory immediate recall ( 16% ). Our group… presented higher rates of impairments in processing speed ( 11.7% in FDT- Reading and 10% in FDT- Counting ). The white matter (WM) analyses with DTI * revealed higher axial diffusivity values in post-infected patients compared to controls. * Diffusion tensor imaging tractography , or DTI tractography, is an MRI (magnetic resonance imaging) technique most commonly used to provide imaging of the brain. Our results suggest persistent cognitive impairment and subtle white matter abnormalities in individuals mildly infected , without anxiety or depression symptoms. One intriguing fact is that we observed a high proportion of low average performance in our sample of patients (which has a high average level of education ), including immediate and late verbal episodic memory, phonological and semantic verbal fluency, immediate visuospatial episodic memory, processing speed, and inhibitory control . Although most subjects did not present significant impaired scores compared with the normative data, we speculate that the low average performance affecting different domains may result in a negative impact in everyday life , especially in individuals with high levels of education and cognitive demands .’ ❂ ❦ Note how these findings might negatively affect daily activities that demand sustained cognitive attention and fast reaction times – such as driving a car or motorbike, or piloting a plane. Consider air-traffic control. Consider the impact on healthcare workers whose occupations combine long periods of intense concentration with a need for critical precision. ❂ 📖 (19 Jan 2024 ~ Nature: Scientific Reports) Microstructural brain abnormalities, fatigue, and cognitive dysfunction after mild COVID-19 ➤ © 2024 Nature .
‘ Clinical evidence suggests that SARS-CoV-2 may lead to hypocalcemia, altered bone turnover markers, and a high prevalence of vertebral fractures. ’
❦ We cannot individually assess the risk of infection from poor indoor air quality. Just as we cannot individually assess food safety in restaurants, or fire safety in cinemas, or aviation safety on flights. These are in the control of others, and are regulated for our health and safety. ❂ © 2024 Orla Hegarty . ➲
❦ ‘Acute infections with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cause a respiratory illness that can be associated with systemic immune cell activation and inflammation , widespread multi-organ dysfunction , and thrombosis . Not everyone fully recovers from COVID-19, leading to Long Covid, the treatment of which is a major unmet clinical need. Long Covid can affect people of all ages , follows severe as well as mild disease , and involves multiple organs . Patients with Long Covid display signs of immune dysfunction and exhaustion , persistent immune cell activation , and autoimmune antibody production , which are also pathological features of acute COVID-19. The complement system is crucial for innate immune defense by effecting lytic destruction of invading micro-organisms, but when uncontrolled, it causes cell and vascular damage . The complement cascade is activated by antigen–antibody complexes in the classical pathways or in the lectin pathway by multimeric proteins (lectins) that recognize specific carbohydrate structures, which are also found on the SARS-CoV-2 spike protein that facilitates host cell entry. Both pathways may contribute to the pronounced complement activation in acute COVID-19. Long Covid symptoms include a postexertional exhaustion reminiscent of other post-viral illnesses , such as myalgic encephalomyelitis ( ME ) – chronic fatigue syndrome ( MECFS ) with suspected latent viral reactivation . Antibody titer changes in Long Covid patients indicate an association of fatigue with reactivation of latent Epstein-Barr virus ( EBV ) infections , and Cervia-Hasler et al found that the severity of Long Covid symptoms is associated with cytomegalovirus ( CMV ) reactivation . A better understanding of the connections between viral reactivation, persistent interferon signaling, and autoimmune pathologies promises to yield new insights into the thromboinflammation associated with Long Covid. Although therapeutic interventions with coagulation and complement inhibitors in acute COVID-19 produced mixed results, the pathological features specific for Long Covid suggest potential interventions for clinical testing. Microclots are also observed in ME-CFS patients , indicating crucial interactions between complement, vWF, and coagulation-mediated fibrin formation in post-viral syndromes. A better definition of these interactions in preclinical and clinical settings will be crucial for the translation of new therapeutic concepts in chronic thromboinflammatory diseases .’ ❂ 📖 (18 Jan 2024 ~ Science) Immune damage in Long Covid ➤ © 2024 Wolfram Ruf / Science .
“I would argue that COVID-19 is not a disease of the lungs at all. It seems most likely that it is what we call a vascular and neurologic infection, affecting both nerve endings and our cardiovascular system.”
❦ I met a nice lady – a ward patient – yesterday who, seeing my respirator [high-filtration mask] , promptly put on her surgical mask. So instead of diving straight in to asking what was most concerning her and how I could help, I opened up a bit about infection control in hospitals. I explained how, because of a lack of respirators, March 2020 saw NHS leaders downgrade PPE for all non-ICU staff. ❂ PPE : Personal Protective Equipment. I then reminded her of the amazing DHSC 2020 and 2021 campaigns on airborne transmission of SARS2 (the green-and-black smoke ones) – and I had to point out that every IPC Lead Nurse had since had to switch off their brain and forget what they knew – and while at work, to only protect ICU staff. ❂ DHSC : Department of Health and Social Care (UK). ❂ IPC : Infection Prevention and Control. I explained that the individuals responsible for the original IPC downgrade were now authors of the national manual on IPC (NIPCM), which sets the standard for infection control in hospitals, and this manual states that airborne transmission is ‘not a thing’ for SARS2 (AGP only). ❂ NIPCM : The UK’s National Infection Prevention and Control Manual. ❂ AGP : Aerosol-Generating Procedure, ie. intubation. So hospitals are destined to be unsafe spaces thanks to the NIPCM, and the surgical mask that she was wearing was OK (ish) to help protect me – but did very little to reduce her risk of SARS2 inhalation. However, she was in a single room (an extra, and not meant as a ward-bed space – but you know, >100% occupancy forever means that you need to use your imagination) – and she already had the window open. She was appalled at what healthcare workers were being put through. She was appalled at the on-going lies. She was appalled at the possible level of harm to patients and staff from such lies. She then went on to tell me how a weekend visitor of hers had just tested positive for Covid. She was worried that they had hugged and chatted, and that she might have got infected. She’s a switched on lady, too. Lives with a medic who has the windows open all the time (“It’s freezing at home”). So I explained about the CleanAirStars.com site. About HEPA filtration being a low energy and low-cost way to remove all airborne pathogens, and to make home a safer place for... • Covid • Flu • RSV • Norovirus • Fungi Etc., etc. The list goes on and on. — “Wow, that’s like magic!” We had a very nice chat. And then we talked about her heart. I just wish I could have this same conversation with each and every NHS CEO and IPC Lead Nurse. I’d ask some questions. I’d want to know why they aren’t protecting staff as they should. I’d want to know why they aren’t protecting patients as they should. I’d want them to know that they are in breach of UK legislation. And I’d want to look them in the eye and ask them to show compassion to the powerless: to staff, and patients. Help us please. Do whatever you can to counter the lies, and to help protect the NHS. Thank-you. ❂ © 2024 Dr. David Tomlinson, NHS Consultant Cardiologist ➲ .
❦ ‘Alzheimer’s disease (AD) is acknowledged by the World Health Organisation (WHO) as a global public health concern. AD is the primary cause of dementia and accounts for 50–70% of cases. SARS-CoV-2 can damage the peripheral and the central nervous system (CNS) through both direct and indirect pathways, potentially leaving COVID-19 patients at higher risks for neurological difficulties, including depression, Parkinson’s disease, AD, etc., after recovering from severe symptoms. Patients who recovered from severe COVID-19 infection are more likely to acquire stable neuropsychiatric and neurocognitive conditions like depression, obsessive-compulsive disorder, psychosis, Parkinson’s disease, and Alzheimer’s disease. SARS-CoV-2 infection causes immune system dysfunction, which can lead to suppression of neurogenesis, synaptic damage, and neuronal death, all of which are associated with the aetiology of Alzheimer’s disease. Severe systemic inflammation caused by SARS-CoV-2 is predicted to have long-term negative consequences, such as cognitive impairment. Research has demonstrated that SARS-CoV-2-infected AD patients had a higher mortality rate. In a study from the Department of Neuroscience at the University of Madrid, 204 participants with Frontotemporal Dementia (FTD) and Alzheimer’s disease (AD) were enrolled. According to the study, 15.2% of these individuals had COVID-19 infection, and sadly, 41.9% of those who had the virus died as a result of their illness. COVID-19 causes a secondary effect on underlying brain pathologies, as SARS-CoV-2 has been shown to trigger or accelerate neurodegeneration processes that possibly explain long-term neurodegenerative effects in the elderly population. In response to the impact of COVID-19 in 2020, governments worldwide acted promptly by implementing various public health measures. During this period, people with cognitive impairments such as dementia or AD may have experienced greater stress and anxiety due to sudden changes in the environment and people’s behaviour. It is also significantly harder for AD patients to comprehend and execute defensive measures such as wearing face masks and sanitising frequently. ❂ COVID-19 has generated a worldwide outbreak, resulting in a slew of issues for humans, particularly those suffering from Alzheimer’s disease. Its ability to invade the central nervous system through the hematogenous and neural routes, besides attacking the respiratory system, has the potential to worsen cognitive decline in Alzheimer’s disease patients. The severity of this issue must be highlighted.’ ❂ 📖 (8 Jan 2024 ~ Frontiers in Aging Neuroscience) Unravelling the connection between COVID-19 and Alzheimer’s disease: a comprehensive review ➤ © 2024 Shajahan et al / Frontiers in Aging Neuroscience .
❦ Q . Why is it important for me to know if I have a COVID-19 infection? ❦ A . If you don’t recover well, it can help your doctor to know if you’ve had a COVID-19 infection – so that they can more effectively treat any of your on-going symptoms. It also helps you to be conscious of the fact that contact with other people might hurt, permanently damage, or kill them.
Post-exertional malaise (PEM) is a marked physical or mental fatigue and deterioration of symptoms occurring after physical , cognitive , social or emotional exertion that would have been tolerated previously. Symptoms typically worsen 12 to 48 hours after such activities , and can last for days , weeks or months , making it difficult to manage or predict. PEM is a hallmark symptom of myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS), and is commonly reported by people with Post-COVID-19 Syndrome (PCS/‘Long Covid’). PEM can be mitigated by activity management , or ‘ pacing ’.
❦ Person puts hand in flame. Gets burnt. Knows fire burns flesh. Has a fear of getting burnt in the future, because fire and flesh create undesirable pain. Lives in a permanent state of fear of fire for rest of life? No. Becomes cautious of fire, and takes precautions to not be burnt again. If anybody accuses you of ‘living in fear’ for taking precautions to avoid catching SARS-CoV-2 (Covid-19) again and again, know that you are, in fact, ‘living with sensible caution’ – as you know that the headaches and heart attacks and strokes and plaque build-up in arteries and the killing of one’s own parents and the reduction of your children’s IQ and your daily fatigue and your memory disorders and immune dysregulation and your new-onset susceptibility to other opportunistic viral, bacterial and fungal infections, and your high blood pressure, and your aggressive, new-onset or recurrence of cancer and the rapid, aggressive, new-onset dementia – are all things you should rightly be afraid of. For yourself, and for other people. But SARS-2 is clever. You often only feel the burn weeks or months later, and you don’t make the connection between the time you stuck your hand in a fire and the now-septic wound that has worked its way into the gristle of your fingers. SARS-2 isn’t stupid, you know, and it has had four years of mutating repeatedly inside several billion humans and animals to hone its game while we sit on the lawn and watch our house burn down. ❂ © 2023 C19.Life .
❦ Ms Amanda Pritchard Chief Executive Officer NHS England Sent via email 22 December 2023 Dear Ms Pritchard, Re: Need for revisions to the IPC guidance to protect healthcare workers from COVID-19 Recently, we have been hearing increasing concerns from across our respective memberships about the protection of healthcare workers and patients from COVID-19 , particularly in light of the rise in cases, hospitalisations and deaths that occurred in September and October [2023] . While it was positive to see a reduction in cases and hospitalisations in November which hopefully reflected a reduction in prevalence as well as the effect of the autumn booster programme, we are starting to see early signs that hospitalisations and cases are starting to rise again. There is no room for complacency, particularly as we deal with winter with an NHS under serious strain. In any case, suppressing the virus remains crucial to reduce the risk of new variants of concern . Moreover, the consequences of infection for some individuals remain serious. We have heard from a range of multidisciplinary clinicians from across primary and secondary care express concern about the lack of availability of even the most basic protections in many settings when they are treating patients with confirmed or suspected COVID-19 . Additionally, the BMA’s Patient Liaison Group has shared information about vulnerable patients not attending healthcare settings due to the fear of a possible COVID-19 infection . These are patients, who remain more susceptible to severe disease from COVID-19 and those for whom vaccines are less effective. As we have routinely highlighted, we believe that the existing Infection Prevention Control ( IPC ) Manual for England , and the specific IPC guidance for COVID-19 which preceded it, have contributed to the lack of protection many of our members experience. The manual does appear to recognise that COVID-19 is airborne . It states that Respiratory Protective Equipment ( RPE ), (i.e. a ( FFP ) respirator ) must be considered when treating a patient with a virus spread wholly or partly by the airborne route (2.4). However, it then makes an unclear distinction between viruses spread wholly or partly by the airborne route , and those spread wholly or partly by the airborne or droplet route where RPE is only recommended for so called “Aerosol Generating Procedures” (AGPs) – an outdated concept based on very poor evidence . Specifically , in Appendix 11, it states that a fluid resistant surgical mask ( FRSM ) is adequate protection for the routine care of COVID-19 positive patients (appendix 11), directly contradicting the statement in 2.4. It also seems very odd to make a distinction between viruses that spread only via the airborne route and those spreading via the airborne or droplet route; staff need protection from an airborne virus in both cases , in one they also need to take droplet-based precautions. The HSE’s own research from 2008 confirms a lack of respiratory protection from a FRSM . It is accepted that COVID-19 can be and is spread by the airborne route . The recent evidence given at the UK COVID-19 Inquiry clearly shows that aerosol transmission is a significant , and almost certainly the dominant, route of transmission for COVID-19 . The current guidance is therefore, at the very least, confusing and, at the worst , is recommending inadequate protection for healthcare workers treating COVID-19 patients . This continues to put them and their patients at risk of infection and, in some cases, Long Covid. We are concerned that there has been a lack of stakeholder engagement in recent months to inform updates the IPC Manual. The latest update on 25 October 2023 does not change the recommended PPE for routine care of a patient with COVID-19, although does include a new footnote seven which concerns patients with undiagnosed respiratory illness where coughing and sneezing are significant features but does not mention COVID-19 or provide guidance on recommended PPE or RPE. Stakeholders, including the signatories to this letter are seeking clarity from you about how we can engage with this process to help inform future revisions of the manual and ensure the guidance is clear and recommends adequate protection for healthcare workers. Employers ultimately have the responsibility for the safety of their workforce , under Health and Safety Law , and the IPC Manual for England references the need for risk assessments and the need to follow the hierarchy of controls. Ensuring the protection , so far as reasonably practicable, of staff who are vulnerable through exposure to the virus and any staff or patients who are individually susceptible and at risk of serious illness if they catch COVID-19 , remains a paramount legal obligation . However, the IPC guidance issued by UKHSA is mandatory in all NHS settings and settings where NHS services are provided. This makes it makes it very difficult for NHS Trusts to reconcile the confusing IPC guidance with their statutory duties as employers under health and safety legislation to provide HSE-approved RPE for protection against airborne hazards . This is especially the case as the HSE has opted not to produce its own guidance on the subject. As we deal with winter, when pressure in the NHS intensifies alongside rising flu and other seasonal respiratory viruses, as well as COVID-19, ensuring there are enough staff across the NHS is more important than ever. COVID-19 is likely to still cause significant staff absence , particularly if cases continue to rise in the coming weeks and months. Providing clear and adequate IPC guidance , including on the need for RPE and adequate ventilation , will help protect healthcare workers and patients and reduce staff absence this winter. Providing staff with adequate protection will also better protect patients and will help reassure vulnerable patients they can safely access healthcare . We would appreciate your reassurance that our concerns will be addressed and the relevant IPC guidance will be urgently updated to reflect this, as well as routinely reviewed. We are of course willing to work with your colleagues and the Chief Nursing Officer on IPC guidance. Yours sincerely, Professor Phil Banfield. BMA, Chair of Council. Dr Barry Jones. Chair of Covid Airborne Protection Alliance (CAPA). ❂ 📖 (22 Dec 2023 ~ The British Medical Association & Covid Airborne Protection Alliance) Need for revisions to the IPC guidance to protect healthcare workers from COVID-19 ➤
‘The RCN is urging healthcare employers to assess the risk posed by COVID-19 and put appropriate safeguards in place for patients and staff .’ ❂ ❦ We’ve contacted chief nursing officers in all four UK countries and the UKHSA to find out what action will be taken in response to WHO’s statement on a new COVID-19 variant of interest. The RCN is asking for a revision to current guidelines , to introduce universal implementation of the two measures advised by the World Health Organization (WHO) to help protect healthcare staff against COVID-19. Earlier this week, in light of the new COVID JN.1 variant, WHO advised healthcare workers and health facilities to: implement universal masking in health facilities , as well as appropriate masking , respirators and other personal protective equipment for health workers caring for suspected and confirmed COVID-19 patients ; improve ventilation in health facilities . The existing national infection prevention and control manuals don’t require standardised masking for COVID-19, and decisions on respiratory protective equipment are left to local risk assessments. This is now inconsistent with WHO’s latest advice . We also have concerns about the adequacy of ventilation in general ward and outpatient areas within hospital buildings and believe that action must be taken to assess and improve this. Although evidence suggests that the global public health risks from the new variant are low, WHO has warned that onset of winter could increase the burden of respiratory infections in the Northern hemisphere. This comes when there are already unsustainable pressures on the health service. Figures show that there has been a rise in COVID-19 cases and hospitalisations , and the RCN argues that without proper protections , ill health could continue to rise in nursing staff and impact their ability to deliver safe and effective patient care . WHO has advised that it is continuously monitoring the evidence and will update the JN.1 risk evaluation as needed. The RCN is urging health care employers to assess the risk posed by COVID-19 and put appropriate safeguards in place for patients and staff . Our COVID-19 workplace risk assessment toolkit aims to help assess and manage the risks associated with respiratory infections such as COVID-19, highlights the duties of nursing staff in specific roles (such as health and safety reps), has advice for employers and leaders, and provides the latest information on risk assessment. ❂ 📖 (21 Dec 2023 ~ Royal College of Nursing / RCN Magazine) COVID JN.1 variant: RCN seeks assurance on new PPE advice ➤ © 2023 Royal College of Nursing (RCN).
❦ ‘Due to its rapidly increasing spread , WHO is classifying the variant JN.1 as a separate variant of interest ( VOI ) from the parent lineage BA.2.86 . It was previously classified as VOI as part of BA.2.86 sublineages. Based on the available evidence, the additional global public health risk posed by JN.1 is currently evaluated as low. Despite this, with the onset of winter in the Northern Hemisphere, JN.1 could increase the burden of respiratory infections in many countries. ➲ Read the risk evaluation: ‘Tracking SARS-CoV-2 variants’ . WHO is continuously monitoring the evidence and will update the JN.1 risk evaluation as needed. Current vaccines continue to protect against severe disease and death from JN.1 and other circulating variants of SARS-CoV-2, the virus that causes COVID-19. COVID-19 is not the only respiratory disease circulating. Influenza, RSV and common childhood pneumonia are on the rise. ➲ WHO advises people to take measures to prevent infections and severe disease using all available tools . These include: • Wear a mask when in crowded, enclosed, or poorly ventilated areas, and keep a safe distance from others, as feasible. • Improve ventilation . • Practise respiratory etiquette – covering coughs and sneezes. • Clean your hands regularly. • Stay up-to-date with vaccinations against COVID-19 and influenza, especially if you are at high risk for severe disease. • Stay home if you are sick . • Get tested if you have symptoms, or if you might have been exposed to someone with COVID-19 or influenza. ✻ ➲ For health workers and health facilities , WHO advises : • Universal masking in health facilities , as well as appropriate masking , respirators and other PPE for health workers caring for suspected and confirmed COVID-19 patients . • Improve ventilation in health facilities. Note : Updated 19 Dec 2023 with additional information for health workers and facilities. ’ ❂ 📖 (19 Jan 2023 ~ WHO / World Health Organization) World Health Organization (WHO) Media Advisory for the COVID-19 variant of interest (VOI) JN.1 ➤ © 2023 WHO / World Health Organization. ❦ Date accessed : 11 Jan 2024 .
❦ I am now absolutely convinced that unless we reduce the transmission of Covid-19 through societal non-pharmaceutical interventions (such as cleaning indoor air) and/or the deployment and uptake of second-generation vaccines, attrition of healthcare will reach a tipping point. This tipping point – which may well happen within the next year – will lead to a global decrease in quality of available healthcare services, which in turn will lead to increased morbidity and mortality from all causes. Every government needs to reduce transmission. The denial of this problem will not change the outcome. Policymakers need to understand this. ❂ © 2023 Conor Browne ➲
❦ ‘Al-Aly’s study undertook a comparative analysis of 94 pre-specified health outcomes and found that over 18 months of follow-up, COVID was associated with a “ significantly increased risk ” for 64 of them, or nearly 70% . The disease’s enhanced risk list includes everything from cardiac arrest , stroke , chronic kidney disease , and cognitive impairment to mental health and fatigue , characteristics often associated with long COVID. By comparison, the seasonal flu was associated with increased risk in only 6 of the 94 conditions specified. Further, while COVID increased the risks for almost all the organ systems studied, the flu heightened risk primarily for the pulmonary ( lung ) system . Those findings, Al-Aly says, suggest that “ COVID is really a multi-systemic disease , and flu is more a respiratory virus ”.’ ❂ 📖 (14 Dec 2023 ~ Fortune) COVID-19 v. Flu: A ‘much more serious threat,’ new study into long-term risks concludes ➤ 📖 (14 Dec 2023 ~ The Lancet) Long-term outcomes following hospital admission for COVID-19 versus seasonal influenza: a cohort study ➤ © 2023 Carolyn Barber / Fortune .
❦ “Coughing into one’s sleeve while in shared air is like peeing into one’s swimsuit while in shared water.” ❂ © 2023 Malgorzata Gasperowicz . ➲
❦ Covid Conscious friend’s 40-year-old partying brother gave Covid to their 80-year-old parents. Mother: spent three weeks in the hospital. Father: went into hospice, and died this morning. Forty-year-old brother never went to hospital nor hospice to visit, because “they’re old”, and “what can I do anyway?” He remains maskless. Co-worker who got Covid along with her father at the family reunion... Covid+ father passed out and was found unconscious in his home. Suffered an acute kidney injury; wears a catheter because he can’t ever urinate on his own again; is now in Palliative Care. Co-worker suddenly can’t remember being sick with Covid, nor her father having had Covid and passing out... and is now telling people that he suffered a kidney injury from a slip and a fall. Colleague says on a virtual call: — “Now that the pandemic is over and people have recovered...” She’s been coughing non-stop since July, and can’t figure out “what I’m allergic to”. Friend posts a picture of a box of KN95s [ear-loop FFP2 respirators] that she purchased online with the caption, “Going back to masking. Got them ready. People protect yourself.” Then for the next three weeks posts maskless pictures at a Patti Labelle concert, a wedding, a birthday dinner, a congressional party... I asked her when she’s going to start using the masks that she posted on Facebook. — “When the president mandates us to.” How many people have you talked to about Covid that have had an “Aha moment”, and immediately starts wearing a well-fitted mask and adjusts their behavior long term? The part of the brain that controls emotions like empathy is damaged. The part of the brain that controls cognitive thinking is damaged. Troll behaviour is at an all-time high because people are triggered by you protecting yourself and them. How incredibly bizarre is this behaviour, and almost everyone who is living in this world at this time! ❂ © 2024 Lady Chuan . ➲
❦ As a consequence of their occupation, doctors and other healthcare workers were at higher risk of contracting coronavirus disease 2019 (COVID-19), and more likely to experience severe disease compared to the general population. Post-acute COVID (Long COVID) in UK doctors is a substantial burden. Insufficient respiratory protection could have contributed to occupational disease, with COVID-19 being contracted in the workplace , and resultant post-COVID complications. Although it may be too late to address the perceived determinants of inadequate protection for those already suffering with Long COVID, more investment is needed in rehabilitation and support of those afflicted . ❂ 📖 (11 Dec 2023 ~ Occupational Medicine) Post-acute COVID-19 complications in UK doctors: results of a cross-sectional survey ➤
❦ I’ve often wondered if Covid, a.k.a. SARS-CoV-2, has its own marketing firm. Over the years, we’ve seen annual “campaigns”, if you will. ❊ 2020 : Hide your elderly and disabled! ❦ Covid still kills and disables children , athletes , and working-age adults . ❊ 2021 : Vax and relax! ❦ You can still transmit COVID if vaccinated; the vaccines wane much more quickly than promised; and lack of masking means faster viral evolution via on-going transmission chains. The vaccines only prevent some severe outcomes some of the time . ❊ 2022 : Back to normal, rise and grind! ❦ Forcing a return to offices and schools without proper mitigations in place – such as ventilation , accurate testing and masking – continues to spread Covid. People wonder why “no-one wants to work anymore”. It’s because they’re out sick. ❊ 2023 : Some folks will fall by the wayside. ❦ Anthony Fauci said this in mid-2023. It is intended to normalize continued higher-than-normal rates of death and disability . Please recall that Fauci had to be pushed hard by Larry Kramer to repurpose meds for HIV while he was at the NIH (USA’s National Institutes of Health). ❊ 2024 : There was no way we could have known. ❦ As rates of global disability climb with no long-term antiviral combination therapy approved, the press and the public start to vent frustrations . We absolutely did know – thanks to the basics of exponential functions and mounds of research. ❊ 2025 : Have you considered MAID? ❦ Due to Canadian efforts at successfully delaying care and benefits to living people while pushing medically-assisted intentional death (MAID), Western governments widely adopt the practice as a way of cutting costs. Influencers suggest 65 is “too old”. ❊ 2026 : Your disease, your responsibility. ❦ Government officials assert that it’s your fault if you didn’t wear an N95 [FFP2 respirator] because there was that one time the CDC (USA’s Centers for Disease Control and Prevention) director barely got the word “mask” out on a video in early December 2023. They use it as a reason for blanket denials of benefits . ❊ 2027 : Get adequate rest! ❦ Campaigns designed to educate the public on the benefits of sleep hygiene are ramped up in the face of increased disability. People are encouraged to work fewer hours if they aren’t feeling well, while their employers demand even more. People are tired. ❊ 2028 : Do your homework, kids! ❦ As PISA studies (Programme for International Student Assessment) continue to show global decline in student performance , education officials ignore the cognitive harms of COVID and instead decry cell-phones and “laziness”. Teen suicides increase due to more pressure, but social media is blamed. ❊ I could go on. A different future is possible, but it’s going to require big changes. Ignore the propaganda. Look at the data. Wear an N95 everywhere where people and air mix – and carry extra masks for others if you can. ❂ © 2023 Chalis Montgomery ➲
❦ The reason why most people aren’t taking Covid-19 seriously is because they simply can’t imagine that their public health body would abandon protections and let an incredibly disabling and airborne virus spread wildly. They will be very angry when it becomes clear to them that that’s exactly what has happened. ❂ © 2023 Dr. David Keegan ➲
❦ Always Covid+ Colleague: — “One of the medical groups. One of the groups. One of the groups...” Moderator: — “Is there something you want to share?” Always Covid+ Colleague: — “I was asked something. I don’t know. It has something to do with something.” This is what Covid is doing to the brain. Unfortunately this is not an isolated incident – but something I’m witnessing all day long throughout the company. ❂ © 2023 Lady Chuan ➲
C-19: Archives
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‘ We are drunk-driving in healthcare... with a pathogen that has a 10% fatality rate in that setting. ’
‘ Vaccine effectiveness against SARS-CoV-2 [COVID-19] infection declines markedly with time and Omicron variants . ’
‘ While acute [short-term] symptoms of reinfection are generally milder, the severity and incidence rate of long COVID increase significantly with the number of reinfections . ’
‘ These findings have important implications for understanding the potential impact of COVID-19 on long-term immune function and susceptibility to pathogens . ’
‘ For patients already battling Alzheimer’s disease , studies indicate that Covid can exacerbate brain inflammation , damage immune cells , and accelerate the disease . Even previously healthy older adults face an increased risk of cognitive impairment and new-onset dementia after infection. Mild Covid cases in younger adults have also been linked to brain issues affecting memory and thinking . ’
‘But even people who had not been hospitalized had increased risks of many conditions, ranging from an 8% increase in the rate of heart attacks to a 247% increase in the rate of heart inflammation.’ Nature (2 Aug 2022) ‘Either symptomatic or asymptomatic SARS-CoV-2 infection is associated with increased risk of late cardiovascular outcomes and has causal effect on all-cause mortality in a late post-COVID-19 period.’ The American Journal of Cardiology (15 Sep 2023)
‘The proportions of PACS [PASC/Long Covid] patients experiencing chest pain, palpitation, and hypertension as sequelae were 22% , 18% , and 19% respectively.’
‘Before Omicron, natural infection provided strong and durable protection against reinfection, with minimal waning over time. However, during the Omicron era, protection was robust only for those recently infected, declining rapidly over time and diminishing within a year.’
‘Scientists discover that even mild COVID-19 can alter brain proteins linked to Alzheimer’s disease, potentially increasing dementia risk. COVID-19-positive individuals exhibited lower cognitive test performance compared to controls – equivalent to almost two years of age-related cognitive decline. ’
‘The predominant symptoms , often clustering together, remain fatigue , cognitive disturbance and chest symptoms , including breathlessness , with sleep disorder and anxiety as additional complaints. Many patients with persistent PCS show impaired executive functioning , reduced cognitive processing speed and reduced physical exercise capacity .’
❦ On that 700-day cough... It’s a new thing, but it’s only reserved for inside supermarkets and offices. And pharmacies and hospitals and care homes. Oh, and your living-room. But apart from that, it’s not exactly a deal-breaker. I mean, c’mon. They put up with way worse in the 1900s. © 2024 C19.Life ❂
❦ “If you are letting yourself get infected and taking no precautions against passing it on, you are not a passive bystander for your next infection. You’ve participated in creating it.”
❦ ‘In this population of healthy young adult US Marines with mostly either asymptomatic or mild acute COVID-19, one fourth reported physical , cognitive , or psychiatric long-term sequelae of infection. The Marines affected with PASC [Post-Acute Sequelae of COVID-19 / Post-COVID-19 Complications / ‘Long Covid’] showed evidence of long-term decrease in functional performance suggesting that SARS-CoV-2 infection may negatively affect health for a significant proportion of young adults .’ ❂ ‘Among the 899 participants, 88.8% had a SARS-CoV-2 infection. Almost a quarter (24.7%) of these individuals had at least one COVID-19 symptom that lasted for at least 4 weeks meeting the a priori definition of PASC established for this study. Among those with PASC, 10 had no acute SARS-CoV-2 symptoms after PCR-confirmed infection suggesting that PASC can occur among asymptomatic individuals. Many participants reported that lingering symptoms impaired their productivity at work, caused them to miss work, and/or limited their ability to perform normal duty/activities. Marines with PASC had significantly decreased physical fitness test scores up to approximately one year post-infection with a three-mile run time that averaged in the 65th percentile of the reference cohort. [ PASC was associated with a significantly increased 3-mile run time on the standard Marine fitness test. PASC participants ran 25.1 seconds slower than a pre-pandemic reference cohort composed of 22,612 Marine recruits from 2016 to 2019. A three-mile run evaluates aerobic exercise , overhead lifting of an ammunition can and pull-ups evaluate strength , and shooting a rifle evaluates fine-motor skills .] Scores for events evaluating upper body (pull-ups, crunches, and ammo-can lift) were not significantly reduced by PASC; however, overall physical fitness scores were reduced. ‘The poorer run times and overall scores among PASC participants are indicative of on-going functional effects.’ Standardized health-based assessments for somatization, depression, and anxiety further highlighted the detrimental health effects of PASC. Almost 10% of participants with PASC had PHQ-8 scores ≥10. Increased somatization * has been associated with increased stress, depression, and problems with emotions. * [ Somatization / Somatisation = Medical symptoms caused by psychological stress.] Additionally, PASC participants had higher GAD-7 scores suggesting increased anxiety in a population with unique inherent occupational stressors associated with higher rates of anxiety, depression, and post-traumatic stress disorder. ‘Increased severity of anxiety among those with PASC, combined with greater rates of mental health disorders in general, could portend an ominous combination and should be closely followed.’ Like others, we identified cardiopulmonary symptoms as some of the most prevalent. The high prevalence of symptoms like shortness of breath, difficulty breathing, cough, and fatigue is particularly notable when combined with decreased objective measures of aerobic performance such as running. These results suggest pathology in the cardiopulmonary system. In contrast we observed no reduction in scores assessing strength and marksmanship suggesting the lack of detectable pathology in the neuro-musculoskeletal system. We have previously found in this same cohort that SARS-CoV-2 infection causes prolonged dysregulation of immune cell epigenetic patterns like auto-immune diseases. Based on the reported PASC symptoms, the potential current and future public health implications in this population could be substantial. ‘Chronic health complications from PASC, especially in a young and previously healthy population with a long life expectancy, could decrease work productivity and increase healthcare costs.’ Significant changes in the Years-of-Life lived with a disability can disproportionally increase disability-adjusted life-years, and should be considered when allocating resources and designing policy.’ ❂ 📖 (23 Oct 2024 ~ The Lancet: Regional Health/America) Clinical and functional assessment of SARS-CoV-2 sequelae among young marines – a panel study ➤ © 2024 The Lancet .
❦ If parents, and politicians and teachers, and healthcare workers and public health bodies wanted things to change, all they need do is read . It’s all there. But they don’t. They won’t. And they insist on their medical and scientific flat-earthing – hand-sanitiser for aerosol-transmitted disease – because they prefer the world to be flat. So let them walk off the edge of the world. [ Caveat: The earth is not flat, and doing nothing will not flatten the curve – but walk far enough, and you are likely to fall off a cliff.] © 2024 C19.Life ❂
❦ NHS nurse: — “Shit, I just got a needlestick injury.” ❦ 2024: — “Yeah, well, whatever. We all gotta die of something.” ❂ © 2024 C19.Life .
‘In those school-rooms where ventilation is imperfect and the air impure, six sevenths of the money expended to educate a child is wasted.’ ❂ The Ventilation and Warming of School Buildings (1887) By Gilbert B. Morrison Published by D. Appleton and Company, New York. 1887. Accessed 10 Apr 2024 Preface (p.xxii) ❦ ‘I am fully convinced that people are prematurely dying by thousands simply from a lack of correct and positive convictions concerning impure air; for, when the true nature of a danger is fully appreciated, the requisite means to avert it will generally be found.’ ❂ Chapter II: The Effects Of Breathing Impure Air (pp.20-23) ❦ ‘Impure air is also believed by the best authorities to be one of the principal causes of epidemics. Dr. Carpenter, than whom there is no abler authority, says: “It is impossible for anyone who carefully examines the evidence to hesitate for a moment in the conclusion that the fatality of epidemics is almost invariably in precise proportion to the degree in which an impure atmosphere has been habitually respired.” The Board of Health of New York conclude that forty per cent of all deaths are caused by breathing impure air. In view of such alarming facts, this same board declares: “Viewing the causes of preventable diseases, and their fatal results, we unhesitatingly state that the first sanitary want in New York and Brooklyn is ventilation .” Direct experiment proves that the air in our school-rooms is impure in almost all cases, and in a majority of them to a degree far beyond the danger line. In view of these facts, and the results as proved by the authorities above cited, why is it regarded by the public with such indifference? When a school-house is blown down by a hurricane, killing and maiming a score of children, it is justly regarded as a great calamity; a vacation is given to quiet the excited fears of parents and children; investigating committees are appointed to locate the responsibility, and the faces of the whole populace are blanched with apprehension. Why is this? Why does the intelligent parent send his child to a school-room poorly ventilated and crowded with children, some of whom are breathing into a stagnant air the germs of disease and death, while others, from unwashed bodies, are delivering into it their deadly emanations, and all without a protest on the part of those even who provide proper hygienic conditions at home? It is because the effects of the one are immediate, occupy little time, the number killed can be actually counted, and the exact magnitude of the calamity estimated all at once. In the other case the process is slower, but of far greater extent; the actual results are by the general public less definitely known, and custom and attention to other matters divert the attention, and the deadly destruction of the innocents by impure air goes on silently, constantly, and powerfully. While noisy demonstrations like that of the cyclone attract attention, and inspire fear and terror, it is in the silent forces that the danger lies. Nature’s most destructive forces, as well as her strongest constructive ones, are silent in their operations; but when Science detects a silent, insidious enemy to human welfare, it is not only our duty to assume an attitude of self-defense and self-protection, but it should be regarded as folly not to do so.’ ❦ On high CO₂ levels connected to poor performance in schools: ‘The effects of breathing impure air thus far considered are pathological, but it has its pedagogical and economical aspects. Every observing teacher knows the immediate relation between the vitiated air in the school-room and the work he wishes the pupils to perform. Much of the disappointment of poor lessons and the tendency to disorder are due directly to this cause. The brain unsupplied with a proper amount of pure blood [oxygen] refuses to act, and the will is powerless to arouse the flagging energies; the general feeling of discomfort, dissatisfaction, and unrest which always accompanies a bad state of the blood. From an economical standpoint it would, of course, be impossible to estimate the financial waste of breathing impure air, but it can not but be enormous. In any discussion of the feasibility of incurring the additional expense of the most perfect ventilation, this loss occasioned by the want of such ventilation must not be ignored.’ ❂ Chapter III: The Air (pp.25-26) ❦ On ventilation, air filtration, and the super-spreading of diverse diseases in classrooms: ‘Wherever an unusual amount of unwholesome matter is being evolved, there especially should the purifying conditions be present; air in such places, to remain pure, must be changed in rapid succession, in order that dilution, diffusion, and oxidation may fulfill their legitimate functions. In a school-room the contaminating process can not but be rapid, and wherever ample provision is not made for rapidly changing the air of the room a dangerous condition of affairs is sure to exist. Bacteria of many forms, and spores of fungi, are also found in the air, and all these organisms are known to thrive in the organic impurities found in the air.’ ❂ Chapter IV: Examination Of The Air (p.33) ❦ On measuring CO₂ levels as a proxy to establishing content of (infectious) re-breathed air: ‘A complete analysis of impure air comprehends the quantitative and qualitative tests for carbonic [sic] dioxide, free ammonia, and other nitrogenous matter, oxidizable matters, nitrous and nitric acids, and hydrogen sulphide; but for ordinary practical purposes the determination of the CO₂ is by far the most important, and is ordinarily the only one which need be made. While the poisonous qualities of the air are not wholly due to the presence of the CO₂ per se, the amount of this gas found to be present is, in air made impure by respiration, generally a good measure for other impurities to which the poisonous quality is principally due. Owing to this fact, a careful test for the amount of CO₂ contained in a given atmosphere is generally the only one which need be made where air is tested merely to determine its respiratory purity.’ ❂ 📖 (Accessed 10 Apr 2024 ~ D. Appleton & Company / Google Books) The Ventilation and Warming of School Buildings ➤ ❂ My thanks to Maarten De Cock for alerting me to this gem of a book. ➲
❦ SARS-CoV-2 – the virus that causes Covid-19 – is airborne . In May 2021, the WHO officially recognised that SARS-CoV-2 is airborne via microscopic aerosols – meaning that the virus is transmissible through the air at both long and short range .
‘ Reinfection , which is now the dominant type of SARS-CoV-2 infection , is not inconsequential ; it can trigger de novo Long Covid or exacerbate its severity . Each reinfection contributes additional risk of Long Covid: cumulatively , two infections yield a higher risk of Long Covid than one infection , and three infections yield a higher risk than two infections .’
❦ This study confirms everything that I have seen in the microscope over the last few years. The authors of the study use a technique called dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI), an imaging technique that can measure the density, integrity, and leakiness of tissue vasculature. Comparing all individuals with previous COVID infection to unaffected controls revealed decreased general brain volume in patients with brain fog along with significantly reduced cerebral white matter volume in both hemispheres in the recovered and brain fog cohorts . Covid-19 induces brain volume loss and leaky blood-brain barrier in some patients. How can this be more clear? © 2024 Danielle Beckman. ➲ ❂ 📖 (22 Feb 2024 ~ Nature: Neuroscience) Blood–brain barrier disruption and sustained systemic inflammation in individuals with long COVID-associated cognitive impairment ➤ 📖 (22 Feb 2024 ~ Nature: Neuroscience) Leaky blood–brain barrier in long-COVID-associated brain fog ➤ ➲ Layperson overview: 📖 (February 2024 ~ Genetic Engineering and Biotechnology News) Leaky Blood Vessels in the Brain Linked to Brain Fog in Long COVID Patients ➤ Related: 📖 (7 Feb 2022 ~ Nature: Cardiovascular Research) Blood–brain barrier link to human cognitive impairment and Alzheimer’s disease ➤ ❂ © 2024 Nature .
‘The very first canon of nursing... the first essential to the patient... is this: to keep the air he breathes as pure as the external air, without chilling him .’ ❂ Notes on Nursing (1860 edition) By Florence Nightingale First Published 1859. Revised edition reprinted in 1860 by Harrison of Pall Mall Accessed 19 Feb 2024 ❦ Chapter I – Ventilation and Warming ‘The very first canon of nursing, the first and the last thing upon which a nurse’s attention must be fixed, the first essential to the patient, without which all the rest you can do for him is as nothing, with which I had almost said you may leave all the rest alone, is this: TO KEEP THE AIR HE BREATHES AS PURE AS THE EXTERNAL AIR, WITHOUT CHILLING HIM. Yet what is so little attended to? Even where it is thought of at all, the most extraordinary misconceptions reign about it. Even in admitting air into the patient’s room or ward, few people ever think where that air comes from. It may come from a corridor into which other wards are ventilated, from a hall, always unaired, always full of the fumes of gas, dinner, of various kinds of mustiness; from an underground kitchen, sink, wash-house, water-closet, or even, as I myself have had sorrowful experience, from open sewers loaded with filth; and with this the patient’s room or ward is aired, as it is called – poisoned, it should rather be said. Always air from the air without, and that, too, through those windows, through which the air comes freshest. From a closed court, especially if the wind do not blow that way, air may come as stagnant as any from a hall or corridor. I know an intelligent humane house surgeon who makes a practice of keeping the ward windows open. The physicians and surgeons invariably close them while going their rounds; and the house surgeon, very properly, as invariably opens them whenever the doctors have turned their backs. I have known a medical officer keep his ward windows hermetically closed, thus exposing the sick to all the dangers of an infected atmosphere, because he was afraid that, by admitting fresh air, the temperature of the ward would be too much lowered. This is a destructive fallacy. To attempt to keep a ward warm at the expense of making the sick repeatedly breathe their own hot, humid, putrescing atmosphere is a certain way to delay recovery or to destroy life.’ ❂ ‘I have known cases of hospital pyæmia quite as severe in handsome private houses as in any of the worst hospitals, and from the same cause, viz., foul air. Yet nobody learnt the lesson. Nobody learnt anything at all from it.’ ❂ ✪ C-19: On schools ‘Of all places, public or private schools, where a number of children or young persons sleep in the same dormitory * , require this test of freshness to be constantly applied.’ * [ C-19 Note: You might substitute ‘sleep’ and ‘dormitory’ with ‘study’ and ‘classroom’ in this section.] ‘If it be hazardous for two children to sleep together in an unventilated bedroom, it is more than doubly so to have four, and much more than trebly so to have six under the same circumstances. People rarely remember this; yet, if parents were as solicitous about the air of school bedrooms as they are about the food the children are to eat, and the kind of education they are to receive, at school, depend upon it due attention would be bestowed on this vitally important matter, and they would cease to have their children sent home either ill, or because scarlet fever or some other “current contagion” had broken out in the school. There are schools where attention is paid to these things, and where “children’s epidemics” are unknown.’ ❂ ✪ C-19: Offices, shops, factories, and other workplaces ‘How much sickness, death, and misery are produced by the present state of many factories, warehouses, workshops, and workrooms!’ ‘How much sickness, death, and misery are produced by the present state of many factories, warehouses, workshops, and workrooms! The places where poor dressmakers, tailors, letter-press printers, and other similar trades have to work for their living, are generally in a worse sanitary condition than any other portion of our worst towns. Many of these places of work were never constructed for such an object. They are badly adapted garrets, sitting-rooms, or bedrooms, generally of an inferior class of house. No attention is paid to cubic space or ventilation. The poor workers are crowded on the floor to a greater extent than occurs with any other kind of over-crowding. The constant breathing of foul air, saturated with moisture, and the action of such air upon the skin renders the inmates peculiarly susceptible of the impression of cold, which is an index indeed of the danger of pulmonary disease to which they are exposed. The result is, that they make bad worse, by over-heating the air and closing up every cranny through which ventilation could be obtained. In such places, and under such circumstances of constrained posture, want of exercise, hurried and insufficient meals, long exhausting labour and foul air – is it wonderful that a great majority of them die early of chest disease, generally of consumption? Intemperance is a common evil of these workshops. The men can only complete their work under the influence of stimulants, which help to undermine their health and destroy their morals, while hurrying them to premature graves. Employers rarely consider these things. Healthy workrooms are no part of the bond into which they enter with their work-people. They pay their money, which they reckon their part of the bargain. And for this wage the workman or workwoman has to give work, health, and life. Do men and women who employ fashionable tailors and milliners ever think of these things? And yet the master is no gainer. His goods are spoiled by foul air and gas fumes, his own health and that of his family suffers, and his work is not so well done as it would be, were his people in health. And the time will come when it will be found cheaper to supply shops, warehouses, and work-rooms with pure air than with foul air.’ ‘And the time will come when it will be found cheaper to supply shops, warehouses, and work-rooms with pure air than with foul air.’ ❂ ✪ C-19: On ‘air-tests’, and measuring CO₂ as a proxy for estimating prevalence of airborne disease indoors ‘Dr. Angus Smith’s air-test, if it could be made of simple application, would be invaluable to use in every sleeping and sick room. Just as without the use of a thermometer no nurse should ever put a patient into a bath, so, if this air-test were made in some equally simple form, should no nurse, or mother, or superintendent, be without it in any ward, nursery, or sleeping-room. But to be used, the air-test must be made as simple a little instrument as the thermometer, and both should be self-registering. ‘...the air-test must be made as simple a little instrument as the thermometer, and both should be self-registering.’ The senses of nurses and mothers become so dulled to foul air that they are perfectly unconscious of what an atmosphere they have let their children, patients, or charges sleep in. But if the tell-tale air-test were to exhibit in the morning, both to nurses and patient and to the superior officer going round, what the atmosphere has been during the night, I question if any greater security could be afforded against a recurrence of the misdemeanour.’ ❂ ✪ C-19: ... And back to the school-room, testing its air, and combatting airborne pathogens ‘And, oh! the crowded national school! where so many children’s epidemics have their origin; and the crowded, unventilated work-room, which sends so many consumptive men and women to the grave; what a tale its air-test would tell! We should have parents saying, and saying rightly, “I will not send my child to that school. I will not trust my son or my daughter in that tailor’s or milliner’s workshop, the air-test stands at ‘Horrid.’” ‘We should have parents saying, and saying rightly, “I will not send my child to that school... the air-test stands at Horrid .”’ And the dormitories of our great boarding schools! Scarlet fever would be no more ascribed to contagion but to its right cause, the air-test standing at “Foul.” We should hear no longer of “mysterious dispensations,” nor of “plague and pestilence” being “in God’s hands,” when, so far as we know, He has put them into our own. The little air-test would both betray the cause of these “mysterious pestilences,” and call upon us to remedy it.’ ❂ ❦ Chapter II – Health of Houses ‘There are five essential points in securing the health of houses:– Pure air. Pure water. Efficient drainage. Cleanliness. Light. Without these, no house can be healthy. And it will be unhealthy just in proportion as they are deficient. To have pure air, your house must be so constructed as that the outer atmosphere shall find its way with ease to every corner of it. ‘To have pure air, your house must be so constructed as that the outer atmosphere shall find its way with ease to every corner of it.’ House architects hardly ever consider this. The object in building a house is to obtain the largest interest for the money, not to save doctor’s bills to the tenants. But, if tenants should ever become so wise as to refuse to occupy unhealthily constructed houses, and if Insurance Companies should ever come to understand their interest so thoroughly as to pay a Sanitary Surveyor to look after the houses where their clients live, speculative architects would speedily be brought to their senses. As it is, they build what pays best. And there are always people foolish enough to take the houses they build. And if in the course of time the families die off, as is so often the case, nobody ever thinks of blaming any but Providence for the result. Ill-informed medical men aid in sustaining the delusion, by laying the blame on “current contagions”. Badly constructed houses do for the healthy what badly constructed hospitals do for the sick.’ ‘Badly constructed houses do for the healthy what badly constructed hospitals do for the sick.’ ❂ ❦ Conclusion ‘The whole of the preceding remarks apply even more to children and to puerperal women than to patients in general. They also apply to the nursing of surgical, quite as much as to that of medical cases. Indeed, if it be possible, cases of external injury require such care even more than sick. In surgical wards, one duty of every nurse certainly is prevention. Fever, or hospital gangrene, or pyæmia, or purulent discharge of some kind may else supervene. If she allows her ward to become filled with the peculiar close fœtid smell, so apt to be produced among surgical cases, especially where there is great suppuration and discharge, she may see a vigorous patient in the prime of life gradually sink and die where, according to all human probability, he ought to have recovered. The surgical nurse must be ever on the watch, ever on her guard, against want of cleanliness, foul air, want of light, and of warmth.’ ‘In surgical wards, one duty of every nurse certainly is prevention.’ ❂ 📖 (Accessed 19 Feb 2024 ~ Original text copied from FiftyWordsForSnow.com) Notes on Nursing (1860) ➤ 📖 (Accessed 19 Feb 2024 ~ Original scanned pages from Google Books) Notes on Nursing (1860) ➤ ❂
❦ LitCovid is the most comprehensive online resource on SARS-CoV-2 / COVID-19, providing access to 417,800+ relevant articles on PubMed. The library of scientific articles is updated daily, and categorised by different research topics (e.g. transmission), as well as geographic locations. ➲ Date accessed: 18 Feb 2024 . ❂ ❦ Useful Categories ✪ Transmission ➤ Characteristics and modes of SARS-CoV-2 transmission. ✪ Prevention ➤ Prevention, control, response and management strategies. ✪ Long Covid ➤ Post-COVID-19 Conditions/Complications (PCC) / Post-Acute Sequelae of COVID-19 (PASC). ✪ Case Reports ➤ Descriptions of specific patient cases. ✪ Treatments ➤ Treatment strategies, therapeutic procedures, and vaccine development. ✪ Forecasting ➤ Modelling, and estimating the trend of SARS-CoV-2 spread. ❂ ➲ LitCovid Online Library ➤ © 2024 National Institutes for Health (NIH) / National Center for Biotechnology Information (NCBI) / U.S. National Library of Medicine (NLM USA).
❦ Mitigation = ‘Lessening the force or intensity of something unpleasant; the act of making a condition or consequence less severe.’ 1. Clean indoor air . The priority should be air filters in schools and hospitals . New ventilation and air filtration standards for all public spaces . Grants made available to businesses to upgrade ventilation and air filtration . 2. FFP2/3 [N95/N99] respirators (masks) in all healthcare settings . 3. Free Covid vaccines available to everyone. 4. Wider access to Covid anti-viral treatments . 5. Free LFT/PCR testing . 6. Improved Covid surveillance , including wastewater monitoring and Long Covid prevalence . 7. Paid sick-leave , so that people don’t go to work when ill. 8. Respirators (masks) on public transport , including flights . 9. Better support and treatments for Long Covid patients . ... and last, but by no means least: 10. A public education campaign on the long-term risks of Covid – and why people should do more to protect themselves. ❦ Addendum : Allocate adequate research funding for a sterilising vaccine as well as treatments/cure for Long Covid . ❂ © 2024 Cat in the Hat . ➲
❦ ‘The occurrences of respiratory disorders among patients who survived for 30 days after the COVID-19 diagnosis continued to rise consistently, including asthma , bronchiectasis , COPD , ILD , PVD * , and lung cancer . * COPD = Chronic obstructive pulmonary disease . ILD = Interstitial lung disease . PVD = Peripheral vascular disease . With the severity of the acute phase of COVID-19, the risk of all respiratory diseases increases progressively. Besides, during the 24-months follow-up, we observed an increasing trend in the risks of asthma and bronchiectasis over time, which indicates that long-term monitoring and meticulous follow-up of these patients is essential. These findings contribute to a more complete understanding of the impact of COVID-19 on the respiratory system and highlight the importance of prevention and early intervention of these respiratory sequelae of COVID-19. In this study, several key findings have been further identified. Firstly, our research demonstrates a significant association between COVID-19 and an increased long-term risk of developing various respiratory diseases. Secondly, we found that the risk of respiratory disease increases with severity in patients with COVID-19, indicating that it is necessary to pay attention to respiratory COVID-19 sequelae in patients, especially those hospitalized during the acute stage of infection. This is consistent with the findings of Lam et al., who found that the risk of some respiratory diseases (including chronic pulmonary disease, acute respiratory distress syndrome and ILD) increased with the severity of COVID-19. Notably, however, our study found that asthma and COPD remained evident even in the non-hospitalized population. This emphasizes that even in cases of mild COVID-19, the healthcare system should remain vigilant. Thirdly, we investigated differences in risk across time periods, as well as the long-term effects of COVID-19 on respiratory disease. During the 2-years follow-up period, the risks of COPD, ILD, PVD and lung cancer decreased, while risks of asthma and bronchiectasis increased. Fourthly, our study showed a significant increase of the long-term risk of developing asthma, COPD, ILD, and lung cancer diseases among individuals who suffered SARS-CoV-2 reinfection. This finding emphasizes the importance of preventing reinfection of COVID-19 in order to protect public health and reduce the potential burden of SARS-CoV-2 reinfection. Interestingly, vaccination appears to have a potentially worsening effect on asthma morbidity compared with other outcomes. This observation aligns with some previous studies that have suggested a possible induction of asthma onset or exacerbation by COVID-19 vaccination. It suggests that more care may be necessary for patients with asthma on taking the COVID vaccines. The underlying mechanisms associated with COVID and respiratory outcomes are not fully understood, but several hypotheses have been proposed. First, SARS-CoV-2 can persist in tissues (including the respiratory tract), as well as the circulating system for an extended period of time after the initial infection. This prolonged presence of the virus could directly contribute to long-term damage of the respiratory tissues, consequently leading to the development of various respiratory diseases. Second, it has been observed that SARS-CoV-2 infection can lead to prolonged immunological dysfunctions, including highly activated innate immune cells, a deficiency in naive T and B cells, and increased expression of interferons and other pro-inflammatory cytokines. These immune system abnormalities are closely associated with common chronic respiratory diseases – asthma, bronchiectasis, COPD, as well as the development of lung cancer. Next, SARS-CoV-2 itself has been shown to drive cross-reactive antibody responses, and a range of autoantibodies were found in patients with COVID-19. In conclusion, our research adds to the existing knowledge regarding the effects of COVID-19 on the respiratory system. Specifically, it shows that the risk of respiratory illness increases with the severity of infection and reinfection. Our findings emphasize the importance of providing extended care and attention to patients previously infected with SARS-CoV-2.’ ❂ 📖 (17 Feb 2024 ~ The Lancet: eClinical Medicine) Long-term risks of respiratory diseases in patients infected with SARS-CoV-2: a longitudinal, population-based cohort study ➤ © 2024 The Lancet: eClinical Medicine .
❦ Chronic disease is like the perfect medical crime. The cause is usually long gone by the time the disease manifests, and nobody links the two until it’s much too late for most. ❂ © 2024 Henry Madison . ➲
❦ It’s really not in the interest of the virus to kill us quickly. That’s why it has mutated to immune escape. That way it enters silently, and then eats you slowly whilst you’re still a spreading vector. Refrigerator trucks are long gone. That’s all the political class wanted. The unseen costs of CVD [cardiovascular disease] , DM [diabetes mellitus] , and both dementia and Parkinson’s Disease are the train coming down the tunnel. The economists are catching up. The actuaries are already there. Politicians and most people? Not yet... ❂ © 2024 Dr. David Joffe, PhD, FRACP / Respiratory Physician ➲ .
❦ “I was in hospital for tests this morning. A nurse asked me: — “How come so many people are wearing masks? Is there something I don’t know?” I almost lost the power of speech.” ❂ © 2024 George Monbiot . ➲
❦ Genomic epidemiology of SARS-CoV-2 with subsampling focused globally since pandemic start. ➲ Built with nextstrain/ncov . Maintained by the Nextstrain team . Enabled by data from GISAID . ➲ Data updated: 21 Jan 2024. ➲ Date accessed: 21 Jan 2024. ❂ © 2024 NextStrain.org ➲
❦ “Every single case in which a person with COVID-19 infects another person in a healthcare setting – patient, relative, or hospital staff member – is a significant failure of hospital procedures. Every single instance .” ❂ © 2024 Professor Steve Robson MPH MD PhD ~ President, Australian Medical Association (AMA) . ➲
❦ Mike Honey’s Variant Visualiser (COVID-19 Genomic Sequence Analysis). The region of ‘Oceania/Australia’ is set by default, as the visualiser was created by Mike Honey , a Data Visualisation and Data Integration specialist in Melbourne, Australia. ➲ Choose your country by clicking on the ‘ Continent, Country, Location ’ dropdown menu in the top-right-hand corner . The variant visualiser is free to use, and is automatically updated every time you open the link. ❂ © 2024 Mike Honey .
❦ ‘Although some studies have shown neuroimaging and neuropsychological alterations in post-COVID-19 patients, fewer combined neuroimaging and neuropsychology evaluations of individuals who presented a mild acute infection. Here we investigated cognitive dysfunction and brain changes in a group of mildly infected individuals. We conducted a cross-sectional study of 97 consecutive subjects ( median age of 41 years ) without current or history of psychiatric symptoms (including anxiety and depression) after a mild infection , with a median of 79 days (and mean of 97 days ) after diagnosis of COVID-19. We performed semi-structured interviews, neurological examinations, 3T-MRI scans, and neuropsychological assessments. The patients reported memory loss ( 36% ), fatigue ( 31% ) and headache ( 29% ). The quantitative analyses confirmed symptoms of fatigue ( 83% of participants), excessive somnolence ( 35% ), impaired phonemic verbal fluency ( 21% ), impaired verbal categorical fluency ( 13% ) and impaired logical memory immediate recall ( 16% ). Our group… presented higher rates of impairments in processing speed ( 11.7% in FDT- Reading and 10% in FDT- Counting ). The white matter (WM) analyses with DTI * revealed higher axial diffusivity values in post-infected patients compared to controls. * Diffusion tensor imaging tractography , or DTI tractography, is an MRI (magnetic resonance imaging) technique most commonly used to provide imaging of the brain. Our results suggest persistent cognitive impairment and subtle white matter abnormalities in individuals mildly infected , without anxiety or depression symptoms. One intriguing fact is that we observed a high proportion of low average performance in our sample of patients (which has a high average level of education ), including immediate and late verbal episodic memory, phonological and semantic verbal fluency, immediate visuospatial episodic memory, processing speed, and inhibitory control . Although most subjects did not present significant impaired scores compared with the normative data, we speculate that the low average performance affecting different domains may result in a negative impact in everyday life , especially in individuals with high levels of education and cognitive demands .’ ❂ ❦ Note how these findings might negatively affect daily activities that demand sustained cognitive attention and fast reaction times – such as driving a car or motorbike, or piloting a plane. Consider air-traffic control. Consider the impact on healthcare workers whose occupations combine long periods of intense concentration with a need for critical precision. ❂ 📖 (19 Jan 2024 ~ Nature: Scientific Reports) Microstructural brain abnormalities, fatigue, and cognitive dysfunction after mild COVID-19 ➤ © 2024 Nature .
‘ Clinical evidence suggests that SARS-CoV-2 may lead to hypocalcemia, altered bone turnover markers, and a high prevalence of vertebral fractures. ’
❦ We cannot individually assess the risk of infection from poor indoor air quality. Just as we cannot individually assess food safety in restaurants, or fire safety in cinemas, or aviation safety on flights. These are in the control of others, and are regulated for our health and safety. ❂ © 2024 Orla Hegarty . ➲
❦ ‘Acute infections with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cause a respiratory illness that can be associated with systemic immune cell activation and inflammation , widespread multi-organ dysfunction , and thrombosis . Not everyone fully recovers from COVID-19, leading to Long Covid, the treatment of which is a major unmet clinical need. Long Covid can affect people of all ages , follows severe as well as mild disease , and involves multiple organs . Patients with Long Covid display signs of immune dysfunction and exhaustion , persistent immune cell activation , and autoimmune antibody production , which are also pathological features of acute COVID-19. The complement system is crucial for innate immune defense by effecting lytic destruction of invading micro-organisms, but when uncontrolled, it causes cell and vascular damage . The complement cascade is activated by antigen–antibody complexes in the classical pathways or in the lectin pathway by multimeric proteins (lectins) that recognize specific carbohydrate structures, which are also found on the SARS-CoV-2 spike protein that facilitates host cell entry. Both pathways may contribute to the pronounced complement activation in acute COVID-19. Long Covid symptoms include a postexertional exhaustion reminiscent of other post-viral illnesses , such as myalgic encephalomyelitis ( ME ) – chronic fatigue syndrome ( MECFS ) with suspected latent viral reactivation . Antibody titer changes in Long Covid patients indicate an association of fatigue with reactivation of latent Epstein-Barr virus ( EBV ) infections , and Cervia-Hasler et al found that the severity of Long Covid symptoms is associated with cytomegalovirus ( CMV ) reactivation . A better understanding of the connections between viral reactivation, persistent interferon signaling, and autoimmune pathologies promises to yield new insights into the thromboinflammation associated with Long Covid. Although therapeutic interventions with coagulation and complement inhibitors in acute COVID-19 produced mixed results, the pathological features specific for Long Covid suggest potential interventions for clinical testing. Microclots are also observed in ME-CFS patients , indicating crucial interactions between complement, vWF, and coagulation-mediated fibrin formation in post-viral syndromes. A better definition of these interactions in preclinical and clinical settings will be crucial for the translation of new therapeutic concepts in chronic thromboinflammatory diseases .’ ❂ 📖 (18 Jan 2024 ~ Science) Immune damage in Long Covid ➤ © 2024 Wolfram Ruf / Science .
“I would argue that COVID-19 is not a disease of the lungs at all. It seems most likely that it is what we call a vascular and neurologic infection, affecting both nerve endings and our cardiovascular system.”
❦ I met a nice lady – a ward patient – yesterday who, seeing my respirator [high-filtration mask] , promptly put on her surgical mask. So instead of diving straight in to asking what was most concerning her and how I could help, I opened up a bit about infection control in hospitals. I explained how, because of a lack of respirators, March 2020 saw NHS leaders downgrade PPE for all non-ICU staff. ❂ PPE : Personal Protective Equipment. I then reminded her of the amazing DHSC 2020 and 2021 campaigns on airborne transmission of SARS2 (the green-and-black smoke ones) – and I had to point out that every IPC Lead Nurse had since had to switch off their brain and forget what they knew – and while at work, to only protect ICU staff. ❂ DHSC : Department of Health and Social Care (UK). ❂ IPC : Infection Prevention and Control. I explained that the individuals responsible for the original IPC downgrade were now authors of the national manual on IPC (NIPCM), which sets the standard for infection control in hospitals, and this manual states that airborne transmission is ‘not a thing’ for SARS2 (AGP only). ❂ NIPCM : The UK’s National Infection Prevention and Control Manual. ❂ AGP : Aerosol-Generating Procedure, ie. intubation. So hospitals are destined to be unsafe spaces thanks to the NIPCM, and the surgical mask that she was wearing was OK (ish) to help protect me – but did very little to reduce her risk of SARS2 inhalation. However, she was in a single room (an extra, and not meant as a ward-bed space – but you know, >100% occupancy forever means that you need to use your imagination) – and she already had the window open. She was appalled at what healthcare workers were being put through. She was appalled at the on-going lies. She was appalled at the possible level of harm to patients and staff from such lies. She then went on to tell me how a weekend visitor of hers had just tested positive for Covid. She was worried that they had hugged and chatted, and that she might have got infected. She’s a switched on lady, too. Lives with a medic who has the windows open all the time (“It’s freezing at home”). So I explained about the CleanAirStars.com site. About HEPA filtration being a low energy and low-cost way to remove all airborne pathogens, and to make home a safer place for... • Covid • Flu • RSV • Norovirus • Fungi Etc., etc. The list goes on and on. — “Wow, that’s like magic!” We had a very nice chat. And then we talked about her heart. I just wish I could have this same conversation with each and every NHS CEO and IPC Lead Nurse. I’d ask some questions. I’d want to know why they aren’t protecting staff as they should. I’d want to know why they aren’t protecting patients as they should. I’d want them to know that they are in breach of UK legislation. And I’d want to look them in the eye and ask them to show compassion to the powerless: to staff, and patients. Help us please. Do whatever you can to counter the lies, and to help protect the NHS. Thank-you. ❂ © 2024 Dr. David Tomlinson, NHS Consultant Cardiologist ➲ .
❦ ‘Alzheimer’s disease (AD) is acknowledged by the World Health Organisation (WHO) as a global public health concern. AD is the primary cause of dementia and accounts for 50–70% of cases. SARS-CoV-2 can damage the peripheral and the central nervous system (CNS) through both direct and indirect pathways, potentially leaving COVID-19 patients at higher risks for neurological difficulties, including depression, Parkinson’s disease, AD, etc., after recovering from severe symptoms. Patients who recovered from severe COVID-19 infection are more likely to acquire stable neuropsychiatric and neurocognitive conditions like depression, obsessive-compulsive disorder, psychosis, Parkinson’s disease, and Alzheimer’s disease. SARS-CoV-2 infection causes immune system dysfunction, which can lead to suppression of neurogenesis, synaptic damage, and neuronal death, all of which are associated with the aetiology of Alzheimer’s disease. Severe systemic inflammation caused by SARS-CoV-2 is predicted to have long-term negative consequences, such as cognitive impairment. Research has demonstrated that SARS-CoV-2-infected AD patients had a higher mortality rate. In a study from the Department of Neuroscience at the University of Madrid, 204 participants with Frontotemporal Dementia (FTD) and Alzheimer’s disease (AD) were enrolled. According to the study, 15.2% of these individuals had COVID-19 infection, and sadly, 41.9% of those who had the virus died as a result of their illness. COVID-19 causes a secondary effect on underlying brain pathologies, as SARS-CoV-2 has been shown to trigger or accelerate neurodegeneration processes that possibly explain long-term neurodegenerative effects in the elderly population. In response to the impact of COVID-19 in 2020, governments worldwide acted promptly by implementing various public health measures. During this period, people with cognitive impairments such as dementia or AD may have experienced greater stress and anxiety due to sudden changes in the environment and people’s behaviour. It is also significantly harder for AD patients to comprehend and execute defensive measures such as wearing face masks and sanitising frequently. ❂ COVID-19 has generated a worldwide outbreak, resulting in a slew of issues for humans, particularly those suffering from Alzheimer’s disease. Its ability to invade the central nervous system through the hematogenous and neural routes, besides attacking the respiratory system, has the potential to worsen cognitive decline in Alzheimer’s disease patients. The severity of this issue must be highlighted.’ ❂ 📖 (8 Jan 2024 ~ Frontiers in Aging Neuroscience) Unravelling the connection between COVID-19 and Alzheimer’s disease: a comprehensive review ➤ © 2024 Shajahan et al / Frontiers in Aging Neuroscience .
❦ Q . Why is it important for me to know if I have a COVID-19 infection? ❦ A . If you don’t recover well, it can help your doctor to know if you’ve had a COVID-19 infection – so that they can more effectively treat any of your on-going symptoms. It also helps you to be conscious of the fact that contact with other people might hurt, permanently damage, or kill them.
Post-exertional malaise (PEM) is a marked physical or mental fatigue and deterioration of symptoms occurring after physical , cognitive , social or emotional exertion that would have been tolerated previously. Symptoms typically worsen 12 to 48 hours after such activities , and can last for days , weeks or months , making it difficult to manage or predict. PEM is a hallmark symptom of myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS), and is commonly reported by people with Post-COVID-19 Syndrome (PCS/‘Long Covid’). PEM can be mitigated by activity management , or ‘ pacing ’.
❦ Person puts hand in flame. Gets burnt. Knows fire burns flesh. Has a fear of getting burnt in the future, because fire and flesh create undesirable pain. Lives in a permanent state of fear of fire for rest of life? No. Becomes cautious of fire, and takes precautions to not be burnt again. If anybody accuses you of ‘living in fear’ for taking precautions to avoid catching SARS-CoV-2 (Covid-19) again and again, know that you are, in fact, ‘living with sensible caution’ – as you know that the headaches and heart attacks and strokes and plaque build-up in arteries and the killing of one’s own parents and the reduction of your children’s IQ and your daily fatigue and your memory disorders and immune dysregulation and your new-onset susceptibility to other opportunistic viral, bacterial and fungal infections, and your high blood pressure, and your aggressive, new-onset or recurrence of cancer and the rapid, aggressive, new-onset dementia – are all things you should rightly be afraid of. For yourself, and for other people. But SARS-2 is clever. You often only feel the burn weeks or months later, and you don’t make the connection between the time you stuck your hand in a fire and the now-septic wound that has worked its way into the gristle of your fingers. SARS-2 isn’t stupid, you know, and it has had four years of mutating repeatedly inside several billion humans and animals to hone its game while we sit on the lawn and watch our house burn down. ❂ © 2023 C19.Life .
❦ Ms Amanda Pritchard Chief Executive Officer NHS England Sent via email 22 December 2023 Dear Ms Pritchard, Re: Need for revisions to the IPC guidance to protect healthcare workers from COVID-19 Recently, we have been hearing increasing concerns from across our respective memberships about the protection of healthcare workers and patients from COVID-19 , particularly in light of the rise in cases, hospitalisations and deaths that occurred in September and October [2023] . While it was positive to see a reduction in cases and hospitalisations in November which hopefully reflected a reduction in prevalence as well as the effect of the autumn booster programme, we are starting to see early signs that hospitalisations and cases are starting to rise again. There is no room for complacency, particularly as we deal with winter with an NHS under serious strain. In any case, suppressing the virus remains crucial to reduce the risk of new variants of concern . Moreover, the consequences of infection for some individuals remain serious. We have heard from a range of multidisciplinary clinicians from across primary and secondary care express concern about the lack of availability of even the most basic protections in many settings when they are treating patients with confirmed or suspected COVID-19 . Additionally, the BMA’s Patient Liaison Group has shared information about vulnerable patients not attending healthcare settings due to the fear of a possible COVID-19 infection . These are patients, who remain more susceptible to severe disease from COVID-19 and those for whom vaccines are less effective. As we have routinely highlighted, we believe that the existing Infection Prevention Control ( IPC ) Manual for England , and the specific IPC guidance for COVID-19 which preceded it, have contributed to the lack of protection many of our members experience. The manual does appear to recognise that COVID-19 is airborne . It states that Respiratory Protective Equipment ( RPE ), (i.e. a ( FFP ) respirator ) must be considered when treating a patient with a virus spread wholly or partly by the airborne route (2.4). However, it then makes an unclear distinction between viruses spread wholly or partly by the airborne route , and those spread wholly or partly by the airborne or droplet route where RPE is only recommended for so called “Aerosol Generating Procedures” (AGPs) – an outdated concept based on very poor evidence . Specifically , in Appendix 11, it states that a fluid resistant surgical mask ( FRSM ) is adequate protection for the routine care of COVID-19 positive patients (appendix 11), directly contradicting the statement in 2.4. It also seems very odd to make a distinction between viruses that spread only via the airborne route and those spreading via the airborne or droplet route; staff need protection from an airborne virus in both cases , in one they also need to take droplet-based precautions. The HSE’s own research from 2008 confirms a lack of respiratory protection from a FRSM . It is accepted that COVID-19 can be and is spread by the airborne route . The recent evidence given at the UK COVID-19 Inquiry clearly shows that aerosol transmission is a significant , and almost certainly the dominant, route of transmission for COVID-19 . The current guidance is therefore, at the very least, confusing and, at the worst , is recommending inadequate protection for healthcare workers treating COVID-19 patients . This continues to put them and their patients at risk of infection and, in some cases, Long Covid. We are concerned that there has been a lack of stakeholder engagement in recent months to inform updates the IPC Manual. The latest update on 25 October 2023 does not change the recommended PPE for routine care of a patient with COVID-19, although does include a new footnote seven which concerns patients with undiagnosed respiratory illness where coughing and sneezing are significant features but does not mention COVID-19 or provide guidance on recommended PPE or RPE. Stakeholders, including the signatories to this letter are seeking clarity from you about how we can engage with this process to help inform future revisions of the manual and ensure the guidance is clear and recommends adequate protection for healthcare workers. Employers ultimately have the responsibility for the safety of their workforce , under Health and Safety Law , and the IPC Manual for England references the need for risk assessments and the need to follow the hierarchy of controls. Ensuring the protection , so far as reasonably practicable, of staff who are vulnerable through exposure to the virus and any staff or patients who are individually susceptible and at risk of serious illness if they catch COVID-19 , remains a paramount legal obligation . However, the IPC guidance issued by UKHSA is mandatory in all NHS settings and settings where NHS services are provided. This makes it makes it very difficult for NHS Trusts to reconcile the confusing IPC guidance with their statutory duties as employers under health and safety legislation to provide HSE-approved RPE for protection against airborne hazards . This is especially the case as the HSE has opted not to produce its own guidance on the subject. As we deal with winter, when pressure in the NHS intensifies alongside rising flu and other seasonal respiratory viruses, as well as COVID-19, ensuring there are enough staff across the NHS is more important than ever. COVID-19 is likely to still cause significant staff absence , particularly if cases continue to rise in the coming weeks and months. Providing clear and adequate IPC guidance , including on the need for RPE and adequate ventilation , will help protect healthcare workers and patients and reduce staff absence this winter. Providing staff with adequate protection will also better protect patients and will help reassure vulnerable patients they can safely access healthcare . We would appreciate your reassurance that our concerns will be addressed and the relevant IPC guidance will be urgently updated to reflect this, as well as routinely reviewed. We are of course willing to work with your colleagues and the Chief Nursing Officer on IPC guidance. Yours sincerely, Professor Phil Banfield. BMA, Chair of Council. Dr Barry Jones. Chair of Covid Airborne Protection Alliance (CAPA). ❂ 📖 (22 Dec 2023 ~ The British Medical Association & Covid Airborne Protection Alliance) Need for revisions to the IPC guidance to protect healthcare workers from COVID-19 ➤
‘The RCN is urging healthcare employers to assess the risk posed by COVID-19 and put appropriate safeguards in place for patients and staff .’ ❂ ❦ We’ve contacted chief nursing officers in all four UK countries and the UKHSA to find out what action will be taken in response to WHO’s statement on a new COVID-19 variant of interest. The RCN is asking for a revision to current guidelines , to introduce universal implementation of the two measures advised by the World Health Organization (WHO) to help protect healthcare staff against COVID-19. Earlier this week, in light of the new COVID JN.1 variant, WHO advised healthcare workers and health facilities to: implement universal masking in health facilities , as well as appropriate masking , respirators and other personal protective equipment for health workers caring for suspected and confirmed COVID-19 patients ; improve ventilation in health facilities . The existing national infection prevention and control manuals don’t require standardised masking for COVID-19, and decisions on respiratory protective equipment are left to local risk assessments. This is now inconsistent with WHO’s latest advice . We also have concerns about the adequacy of ventilation in general ward and outpatient areas within hospital buildings and believe that action must be taken to assess and improve this. Although evidence suggests that the global public health risks from the new variant are low, WHO has warned that onset of winter could increase the burden of respiratory infections in the Northern hemisphere. This comes when there are already unsustainable pressures on the health service. Figures show that there has been a rise in COVID-19 cases and hospitalisations , and the RCN argues that without proper protections , ill health could continue to rise in nursing staff and impact their ability to deliver safe and effective patient care . WHO has advised that it is continuously monitoring the evidence and will update the JN.1 risk evaluation as needed. The RCN is urging health care employers to assess the risk posed by COVID-19 and put appropriate safeguards in place for patients and staff . Our COVID-19 workplace risk assessment toolkit aims to help assess and manage the risks associated with respiratory infections such as COVID-19, highlights the duties of nursing staff in specific roles (such as health and safety reps), has advice for employers and leaders, and provides the latest information on risk assessment. ❂ 📖 (21 Dec 2023 ~ Royal College of Nursing / RCN Magazine) COVID JN.1 variant: RCN seeks assurance on new PPE advice ➤ © 2023 Royal College of Nursing (RCN).
❦ ‘Due to its rapidly increasing spread , WHO is classifying the variant JN.1 as a separate variant of interest ( VOI ) from the parent lineage BA.2.86 . It was previously classified as VOI as part of BA.2.86 sublineages. Based on the available evidence, the additional global public health risk posed by JN.1 is currently evaluated as low. Despite this, with the onset of winter in the Northern Hemisphere, JN.1 could increase the burden of respiratory infections in many countries. ➲ Read the risk evaluation: ‘Tracking SARS-CoV-2 variants’ . WHO is continuously monitoring the evidence and will update the JN.1 risk evaluation as needed. Current vaccines continue to protect against severe disease and death from JN.1 and other circulating variants of SARS-CoV-2, the virus that causes COVID-19. COVID-19 is not the only respiratory disease circulating. Influenza, RSV and common childhood pneumonia are on the rise. ➲ WHO advises people to take measures to prevent infections and severe disease using all available tools . These include: • Wear a mask when in crowded, enclosed, or poorly ventilated areas, and keep a safe distance from others, as feasible. • Improve ventilation . • Practise respiratory etiquette – covering coughs and sneezes. • Clean your hands regularly. • Stay up-to-date with vaccinations against COVID-19 and influenza, especially if you are at high risk for severe disease. • Stay home if you are sick . • Get tested if you have symptoms, or if you might have been exposed to someone with COVID-19 or influenza. ✻ ➲ For health workers and health facilities , WHO advises : • Universal masking in health facilities , as well as appropriate masking , respirators and other PPE for health workers caring for suspected and confirmed COVID-19 patients . • Improve ventilation in health facilities. Note : Updated 19 Dec 2023 with additional information for health workers and facilities. ’ ❂ 📖 (19 Jan 2023 ~ WHO / World Health Organization) World Health Organization (WHO) Media Advisory for the COVID-19 variant of interest (VOI) JN.1 ➤ © 2023 WHO / World Health Organization. ❦ Date accessed : 11 Jan 2024 .
❦ I am now absolutely convinced that unless we reduce the transmission of Covid-19 through societal non-pharmaceutical interventions (such as cleaning indoor air) and/or the deployment and uptake of second-generation vaccines, attrition of healthcare will reach a tipping point. This tipping point – which may well happen within the next year – will lead to a global decrease in quality of available healthcare services, which in turn will lead to increased morbidity and mortality from all causes. Every government needs to reduce transmission. The denial of this problem will not change the outcome. Policymakers need to understand this. ❂ © 2023 Conor Browne ➲
❦ ‘Al-Aly’s study undertook a comparative analysis of 94 pre-specified health outcomes and found that over 18 months of follow-up, COVID was associated with a “ significantly increased risk ” for 64 of them, or nearly 70% . The disease’s enhanced risk list includes everything from cardiac arrest , stroke , chronic kidney disease , and cognitive impairment to mental health and fatigue , characteristics often associated with long COVID. By comparison, the seasonal flu was associated with increased risk in only 6 of the 94 conditions specified. Further, while COVID increased the risks for almost all the organ systems studied, the flu heightened risk primarily for the pulmonary ( lung ) system . Those findings, Al-Aly says, suggest that “ COVID is really a multi-systemic disease , and flu is more a respiratory virus ”.’ ❂ 📖 (14 Dec 2023 ~ Fortune) COVID-19 v. Flu: A ‘much more serious threat,’ new study into long-term risks concludes ➤ 📖 (14 Dec 2023 ~ The Lancet) Long-term outcomes following hospital admission for COVID-19 versus seasonal influenza: a cohort study ➤ © 2023 Carolyn Barber / Fortune .
❦ “Coughing into one’s sleeve while in shared air is like peeing into one’s swimsuit while in shared water.” ❂ © 2023 Malgorzata Gasperowicz . ➲
❦ Covid Conscious friend’s 40-year-old partying brother gave Covid to their 80-year-old parents. Mother: spent three weeks in the hospital. Father: went into hospice, and died this morning. Forty-year-old brother never went to hospital nor hospice to visit, because “they’re old”, and “what can I do anyway?” He remains maskless. Co-worker who got Covid along with her father at the family reunion... Covid+ father passed out and was found unconscious in his home. Suffered an acute kidney injury; wears a catheter because he can’t ever urinate on his own again; is now in Palliative Care. Co-worker suddenly can’t remember being sick with Covid, nor her father having had Covid and passing out... and is now telling people that he suffered a kidney injury from a slip and a fall. Colleague says on a virtual call: — “Now that the pandemic is over and people have recovered...” She’s been coughing non-stop since July, and can’t figure out “what I’m allergic to”. Friend posts a picture of a box of KN95s [ear-loop FFP2 respirators] that she purchased online with the caption, “Going back to masking. Got them ready. People protect yourself.” Then for the next three weeks posts maskless pictures at a Patti Labelle concert, a wedding, a birthday dinner, a congressional party... I asked her when she’s going to start using the masks that she posted on Facebook. — “When the president mandates us to.” How many people have you talked to about Covid that have had an “Aha moment”, and immediately starts wearing a well-fitted mask and adjusts their behavior long term? The part of the brain that controls emotions like empathy is damaged. The part of the brain that controls cognitive thinking is damaged. Troll behaviour is at an all-time high because people are triggered by you protecting yourself and them. How incredibly bizarre is this behaviour, and almost everyone who is living in this world at this time! ❂ © 2024 Lady Chuan . ➲
❦ As a consequence of their occupation, doctors and other healthcare workers were at higher risk of contracting coronavirus disease 2019 (COVID-19), and more likely to experience severe disease compared to the general population. Post-acute COVID (Long COVID) in UK doctors is a substantial burden. Insufficient respiratory protection could have contributed to occupational disease, with COVID-19 being contracted in the workplace , and resultant post-COVID complications. Although it may be too late to address the perceived determinants of inadequate protection for those already suffering with Long COVID, more investment is needed in rehabilitation and support of those afflicted . ❂ 📖 (11 Dec 2023 ~ Occupational Medicine) Post-acute COVID-19 complications in UK doctors: results of a cross-sectional survey ➤
❦ I’ve often wondered if Covid, a.k.a. SARS-CoV-2, has its own marketing firm. Over the years, we’ve seen annual “campaigns”, if you will. ❊ 2020 : Hide your elderly and disabled! ❦ Covid still kills and disables children , athletes , and working-age adults . ❊ 2021 : Vax and relax! ❦ You can still transmit COVID if vaccinated; the vaccines wane much more quickly than promised; and lack of masking means faster viral evolution via on-going transmission chains. The vaccines only prevent some severe outcomes some of the time . ❊ 2022 : Back to normal, rise and grind! ❦ Forcing a return to offices and schools without proper mitigations in place – such as ventilation , accurate testing and masking – continues to spread Covid. People wonder why “no-one wants to work anymore”. It’s because they’re out sick. ❊ 2023 : Some folks will fall by the wayside. ❦ Anthony Fauci said this in mid-2023. It is intended to normalize continued higher-than-normal rates of death and disability . Please recall that Fauci had to be pushed hard by Larry Kramer to repurpose meds for HIV while he was at the NIH (USA’s National Institutes of Health). ❊ 2024 : There was no way we could have known. ❦ As rates of global disability climb with no long-term antiviral combination therapy approved, the press and the public start to vent frustrations . We absolutely did know – thanks to the basics of exponential functions and mounds of research. ❊ 2025 : Have you considered MAID? ❦ Due to Canadian efforts at successfully delaying care and benefits to living people while pushing medically-assisted intentional death (MAID), Western governments widely adopt the practice as a way of cutting costs. Influencers suggest 65 is “too old”. ❊ 2026 : Your disease, your responsibility. ❦ Government officials assert that it’s your fault if you didn’t wear an N95 [FFP2 respirator] because there was that one time the CDC (USA’s Centers for Disease Control and Prevention) director barely got the word “mask” out on a video in early December 2023. They use it as a reason for blanket denials of benefits . ❊ 2027 : Get adequate rest! ❦ Campaigns designed to educate the public on the benefits of sleep hygiene are ramped up in the face of increased disability. People are encouraged to work fewer hours if they aren’t feeling well, while their employers demand even more. People are tired. ❊ 2028 : Do your homework, kids! ❦ As PISA studies (Programme for International Student Assessment) continue to show global decline in student performance , education officials ignore the cognitive harms of COVID and instead decry cell-phones and “laziness”. Teen suicides increase due to more pressure, but social media is blamed. ❊ I could go on. A different future is possible, but it’s going to require big changes. Ignore the propaganda. Look at the data. Wear an N95 everywhere where people and air mix – and carry extra masks for others if you can. ❂ © 2023 Chalis Montgomery ➲
