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Autoantibody COVID link ‘potentially game-changing’


Doug Hendrie


14/12/2020 1:42:09 PM

The body’s own response to coronavirus may cause severe cases of COVID and lingering damage to the heart, lungs, brain and other organs.

The novel coronavirus
The SARS-CoV-2 coronavirus continues to surprise researchers.

A preprint study by Yale researchers makes the case that the body’s response to the SARS-CoV-2 coronavirus may be causing the production of autoantibodies – wildcard immune proteins which mistakenly seek out and damage the body’s own systems rather than targeting viruses.
 
The findings could shed more light on the most puzzling aspects of COVID – namely, why a coronavirus can damage so many different parts of the body, and, for many patients, lead to an ongoing array of debilitating symptoms.
 
The study has been dubbed ‘potentially game-changing’ by prominent UK-based Professor of Primary Care Trisha Greenhalgh, and may result in more research into the little-known ways viruses can lead to autoimmune conditions.
 
It involved screening almost 200 patients with the coronavirus, specifically looking for the presence of autoantibodies that work against thousands of the body’s extracellular and secreted proteins. The control group comprised 30 healthcare workers without the virus.
 
The result?
 
In the COVID group, the researchers identified a wide range of autoantibodies, running from uncommon varieties (5–10% prevalence) such as those that attack type 1 interferons, which regulate the immune system, through to rarer autoantibodies (<1–5% prevalence) that work against B cells or T cells, which are critical immune components.
 
‘We found that COVID-19 patients exhibit dramatic increases in autoantibody reactivities compared to uninfected controls, with a high prevalence of autoantibodies against immunomodulatory proteins including cytokines, chemokines, complement components, and cell surface proteins,’ the paper states.
 
Unfortunately, though COVID-19 patients had high reactivity at a global level, there were ‘essentially no “COVID-19 specific” autoantibodies that distinguished COVID-19 patients from uninfected controls,’ the researchers write.
 
Rather, the ‘aggregate sum of these multifarious responses may explain a significant portion of the clinical variation in patients’.
 
To validate these findings, the researchers used surrogates of these antibodies in mice, which led to increased disease severity. 
 
The findings also suggest that patients with pre-existing autoantibodies – such as those with autoimmune disease – would be particularly at risk from severe forms of COVID.
 
Senior author Assistant Professor Aaron Ring told The Guardian that if autoantibodies induced by COVID-19 endured in the body, they might be implicated in long COVID.
 
‘Post-COVID syndromes could plausibly be caused by long-lived autoantibodies that persist well after the virus is cleared from the body,’ he said.
 
‘If this is the case, there are immunosuppressive treatments, such as those used for rheumatological diseases, that could be effective.’
 
At present, long COVID is believed to affect up to 10% of younger people (18–49), with higher rates amongst older people.
 
While some autoantibodies were present before infection, others came into being and grew in number during the course of the disease.
 
Paper co-author Professor Akiko Iwasaki noted on Twitter that the targets of the autoantibodies were very widespread. 
 
‘Some antibodies bound to interferons, chemokine and cytokines, while others bound to proteins expressed on the surface of immune and non-immune cells,’ she wrote.
 
‘In addition to immune-related antigens, we also found antibodies to various tissue-specific antigens in organs like the central nervous system, vascular, connective tissues, liver, [and gastrointestinal] tract. Such antibodies could drive damage in target tissues.’
 
Researchers are increasingly focusing on COVID’s link to autoimmune disease. Surgeon Dr Timothy Icenogle, the author of a recent paper on the topic, told Elemental that we’re ‘gradually coming to the realisation that COVID-19 is primarily an autoimmune disease that is triggered by a virus’.
 
An October study in Nature also found that critically ill COVID patients had all the markers of extrafollicular B cell activation, which ‘correlated strongly with large antibody-secreting cell expansion and early production of high concentrations of SARS-CoV-2-specific neutralising antibodies’.
 
Despite early production of coronavirus antibodies, these patients had ‘severe disease with elevated inflammatory biomarkers, multi-organ failure and death’.
 
‘These findings strongly suggest a pathogenic role for immune activation in subsets of patients with COVID-19,’ the researchers state.
 
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Dr Peter Wells   15/12/2020 12:03:19 PM

What does this mean for possible long term effects of Covi 19 vaccines?