Covid-19: what you need to know today
Covid-19 has been known for some time to affect people (or at least some people) in the same way that autoimmune disorders do. Dispatch 140 on Aug. 25 wrote about this, the challenges it posed, as well as the possible lines of treatment that were available if one were to respond to Covid-19 as one would other autoimmune disorders. Two recent articles, both by researchers at Yale School of Medicine, shed more light on this. My colleague Binayak Dasgupta pointed me in the direction of one, who has made it his mission in recent months to keep track of the latest Covid-19 research, and then correspond with the authors to understand more; he’s my go-to person in the newsroom when I want to discuss the science of just about anything to do with viral infection, from testing to trajectory to vaccinations. The other one appeared on my radar. Both articles are pre-printed on medRxiv and are not peer-reviewed.
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The first article, titled “Diverse Functional Autoantibodies in Covid-19 Patients,” is by Eric Y Wang, Tianyang Mao, Akiko Iwasaki, and others. Several autoimmune diseases are caused by autoantibodies, essentially antibodies that attack the host’s own organs and cells. These autoantibodies target autoantigens, proteins made by the body while doing normal activities or due to infection. And when they target these, they also target the underlying cells, tissues, or organs. The presence of autoantibodies and the role they play could explain why, in the case of some patients, Covid-19 targets various organs and systems (including the immune system), often with fatal consequences. This is what the researchers studied. Using a method called Rapid Extracellular Antigen Profiling, the researchers looked for autoantibodies in 194 Covid-19 patients. They found that “Covid-19 patients exhibit dramatic increases in autoantibody reactivities” compared to the uninfected people in the study, and that these autoantibodies “target a wide range of immune-related proteins.” They also found, using a mouse model (mouse tests) that “antibodies directed at the immune system exacerbate the severity of the disease” and that the presence of autoantibodies directed at “tissue-associated antigens” has a correlation with the severity of the illness.
Why is this important? One, it points (as all good studies do) to new avenues of research, in this case, the role of autoantibodies in the severity of Covid-19 infections. And two, it also points to potential therapies (or, at least, the direction in which they can be found).
Also read: Covid-19 can also have an impact on the heart, experts say
The second article, titled “Post-infectious inflammatory disease in MIS-C exhibits elevated cytotoxicity signatures and self-reactivity that correlates with severity,” is by Anjali Ramaswamy, Nina N Brodsky, Carrie L Lucas, and others. Researchers studied 15 children with MIS-C (multi-system inflammatory syndrome in children), an autoimmune disorder that can cause many organs in the body to become inflamed and is linked to Covid-19. The researchers explain that the syndrome typically manifests itself in young people “who had a mild or asymptomatic Sars-CoV-2 infection approximately 4-6 weeks earlier.” By detecting autoantibodies and using other techniques, the researchers concluded that a “previous Sars-Cov-2 infection causes lasting immune alterations that set the stage for the development of acute and life-threatening inflammation” in some older children.
Understanding the autoimmune aspects of Covid-19, and because of articles like these two, we now know more about these than before, can help to identify and address MIS-C and other syndromes (initially, for example, when the first cases of MIS- C, the doctors believed they were seeing manifestations of Kawasaki disease). It also adds to what we know about prolonged Covid, which was one of the first signs that, at least in some cases, Sars-CoV-2 has the same impact as autoimmune diseases.
We may have created vaccines that effectively prevent Covid-19, but we are still learning about the disease.