It’s been known for a few time that Covid-19 affects people (or a minimum of some people) the way autoimmune disorders do. Dispatch 140 on August 25 wrote about this, the challenges it posed, also because the possible lines of treatment that became available if one were to reply to Covid-19 the way one would to other autoimmune disorders. Two recent papers, both from researchers at the Yale School of drugs , shed more light on this. i used to be pointed within the direction of 1 by my colleague Binayak Dasgupta, who has made it his mission in recent months to stay track of the newest research on Covid-19, then correspond with the authors to know more; he's my go-to person within the newsroom once I want to debate the science of almost anything to try to to with the virus infection – from testing to trajectory to vaccines. the opposite showed abreast of my radar. Both papers are pre-prints on medRxiv, and not peer-reviewed.
The first paper, titled “Diverse Functional Autoantibodies in patients with Covid-19”, is by Eric Y Wang, Tianyang Mao, Akiko Iwasaki, et al. . Several autoimmune diseases are caused by autoantibodies, essentially antibodies that attack the host’s own organs and cells. These autoantibodies target self-antigens, proteins produced by the body because it goes about its normal activities or due to an infection. And once they target these, they also target the underlying cells, tissues or organs. The presence of autoantibodies, and therefore the role played by them could explain why, within the case of some patients, Covid-19 targets several organs and systems (including the immune system), often with fatal consequences. this is often what the researchers studied. employing a method called Rapid Extracellular Antigen Profiling, the researchers checked for autoantibodies in 194 Covid-19 patients. They found that “Covid-19 patients exhibit dramatic increases in autoantibody reactivities” in comparison to uninfected people within the study, which these autoantibodies “target a good range of immune-related proteins”. They also found, employing a mouse model (tests on mice) that “immune-targeting antibodies exacerbate disease severity” which the presence of autoantibodies that focus on “tissue-associated antigens” have a correlation with the severity of the disease.
Why is that this important? One, it points (like all good studies do) to further avenues of research – during this case, the role of autoantibodies within the severity of Covid-19 infections. And two, it also points to possible therapies (or, at least, to the direction during which these could also be found).
The second paper, titled “Post-infectious disease in MIS-C features elevated cytotoxicity signatures and autoreactivity that correlates with severity”, is by Anjali Ramaswamy, Nina N Brodsky, Carrie L Lucas, et al. . The researchers studied 15 children with MIS-C (multisystem inflammatory syndrome in children), an autoimmune disease which will cause many body organs to become inflamed, and which is said to Covid-19. The researchers explain that the syndrome typically manifests itself in children “who had a light or asymptomatic Sars-CoV-2 infection roughly 4-6 weeks prior”. Screening for autoantibodies and using other techniques, the researchers concluded that a “prior Sars-Cov-2 infection causes lasting immune alterations that set the stage for development of an acute and life-threatening” inflammation in some older children.
Understanding the autoimmune aspects of Covid-19 – and since of papers like these two, we now know more about these than we previously did – can help identify and address MIS-C and other syndromes (initially, as an example , when the primary cases of MIS-C emerged, doctors believed they were seeing manifestations of Kawasaki Disease). It also adds to what we all know of long-Covid – which was among the primary signs that, a minimum of in some cases, Sars-CoV-2 has an equivalent impact as autoimmune diseases.
We may have come up with vaccines that effectively prevent Covid-19, but we are still learning about the disease.