SARS-CoV-2 triggering autoimmune diseases

SWAlexander

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Sorry if this has already been posted.

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SARS-CoV-2, the cause of the pandemic coronavirus disease, causes dysregulation of an immune response.

Infection of respiratory epithelium by virus triggers both innate and acquired immunity that led to the immune system's hyperactivation.

Therefore, triggering chronic inflammation can contribute to autoimmune disease.

Post-Covid-19 autoimmunity may be due to molecular mimicry, bystander activation of T cells, transient immunosuppression, and pro-inflammatory cytokines, which might complicate SARS-CoV-2 vaccination.

Abstract
Autoimmunity, hyperstimulation of the immune system, can be caused by a variety of reasons. Viruses are thought to be important environmental elements that contribute to the development of autoimmune antibodies. It seems that viruses cause autoimmunity with mechanisms such as molecular mimicry, bystander activation of T cells, transient immunosuppression, and inflammation, which has also been seen in post-Covid-19 autoimmunity. Infection of respiratory epithelium by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) dysregulates the immune response, triggers both innate and acquired immunity that led to the immune system's hyperactivation, excessive cytokine secretion known as “cytokine storm,” and finally acute respiratory distress syndrome (ARDS) associated with high mortality. Any factor in the body that triggers chronic inflammation can contribute to autoimmune disease, which has been documented during the Covid-19 pandemic. It has been observed that some patients produce autoantibody and autoreactive CD4+ and CD8+ T cells, leading to the loss of self-tolerance. However, there is a scarcity of evidence defining the precise molecular interaction between the virus and the immune system to elicit autoreactivity. Here, we present a review of the relevant immunological findings in Covid-19 and the current reports of autoimmune disease associated with the disease.
https://www.sciencedirect.com/science/article/pii/S1043466622000825?via=ihub

Today I´m convinced that existing immunodeficiency, is the foundation for ME/CFS and is emphasized by either bacteria or viruses.
 

SWAlexander

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Here is a contradiction.

It is not hyper-stimulation - it is "an abnormally suppressed immune system"

Source: University of California - Los Angeles Health Sciences

Summary:
Researchers studying the effect of the monoclonal antibody Leronlimab on long COVID-19 may have found a surprising clue to the baffling syndrome, one that contradicts their initial hypothesis. An abnormally suppressed immune system may be to blame, not a persistently hyperactive one as they had suspected.
A UCLA-led team of researchers studying the effect of the monoclonal antibody Leronlimab on long COVID-19 may have found a surprising clue to the baffling syndrome, one that contradicts their initial hypothesis. An abnormally suppressed immune system may be to blame, not a persistently hyperactive one as they had suspected.

The study, which was funded by Leronlimab maker CytoDyn Inc. and conducted by researchers either employed by or serving as consultants to the company, will be published online April 22 in the peer reviewed journal Clinical Infectious Diseases.
"While this was a small pilot study, it does suggest that some people with long COVID may actually have under-active immune systems after recovering from COVID-19, which means that boosting immunity in those individuals could be a treatment," said senior author Dr. Otto Yang, a professor of medicine, division of infectious diseases, and of microbiology, immunology and molecular genetics at the David Geffen School of Medicine at UCLA.
COVID-19 is known to be caused by hyperactive immune responses against SARS-CoV-2 resulting in damage to lungs and other organs, and sometimes what is known as a "cytokine storm" that overwhelms the individual, which could lead to severe illness and death.
In a subset of persons who recover from the initial illness, various symptoms persist, such as fatigue, mental haziness, and shortness of breath, which can be debilitating and last for months. This is generally classified as long COVID, although symptoms vary widely and this syndrome is probably not a single disease entity. Limited understanding of its causes, however, makes finding ways to treat the condition particularly difficult.
Many scientists have suggested that persistence of immune hyperactivity after COVID-19 is a major contributor. Working under this theory, the researchers conducted a small exploratory trial of Leronlimab -- an antibody that attaches to an immune receptor called CCR5 that is involved in inflammation -- on 55 people with the syndrome.
Participants were randomly assigned to receive weekly injections of the antibody or a saline placebo for eight weeks, over which time they tracked any changes in 24 symptoms associated with long COVID, which also included loss of smell and taste, muscle and joint pain, and brain fog.
The researchers originally thought that blocking CCR5 with the antibody would dampen the activity of an overactive immune system after COVID-19 infection.
"But we found just the opposite," Yang said. "Patients who improved were those who started with low CCR5 on their T cells, suggesting their immune system was less active than normal, and levels of CCR5 actually increased in people who improved. This leads to the new hypothesis that long COVID in some persons is related to the immune system being suppressed and not hyperactive, and that while blocking its activity, the antibody can stabilize CCR5 expression on the cell surface leading to upregulation of other immune receptors or functions."
The findings, the researchers write, "suggests a complex role for CCR5 in balancing inflammatory and anti-inflammatory effects, e.g. through T regulatory cells," although the results need to be confirmed in a larger, more definitive study.
Study co-authors are Norman Gaylis of Arthritis & Rheumatic Disease Specialties in Aventura, Florida; Angela Ritter of the Center for Advanced Research & Education in Gainesville, Georgia; Scott Kelly, Nader Pourhassan, and Christopher Recknor of CytoDyn Inc. in Vancouver, Washington; and Meenakshi Tiwary, Jonah Sacha, and Scott Hansen of Oregon Health & Science University.
continue: https://www.sciencedaily.com/releas...6U4W_m131LXCcizgviNU3rAIcZom0E45Pj6i-qsRLnFmM
 
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If—and it's a big 'if'—that UCLA-led* study is borne out by larger studies, I wonder what that means for ME? And for all the people with ME (like myself) who have well-functioning immune-systems?—I mean the people who have had one cold every 5 years (or even less frequently) since they fell ill with ME, who had no or very limited reactions to the Covid jabs, etc., but have all the other problems.

(*The senior author is Yang.)

Link to study:

https://academic.oup.com/cid/advance-article/doi/10.1093/cid/ciac226/6572226?login=true