Covid-19: What you need to know today
It’s been known for some time that Covid-19 affects people (or at least some people) the way autoimmune disorders do. Dispatch 140 on August 25 wrote about this, the challenges it posed, as well as the possible lines of treatment that became available if one were to respond to Covid-19 the way one would to other autoimmune disorders. Two recent papers, both from researchers at the Yale School of Medicine, shed more light on this. I was pointed in the direction of one by my colleague Binayak Dasgupta, who has made it his mission in recent months to keep track of the latest research on Covid-19, and then correspond with the authors to understand more; he is my go-to person in the newsroom when I want to discuss the science of just about anything to do with the viral infection – from testing to trajectory to vaccines. The other showed up on 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 Both papers are pre-prints on medRxiv, and not peer-reviewed.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, and others. 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 as it goes about its normal activities or because of an infection. And when they target these, they also target the underlying cells, tissues or organs. The presence of autoantibodies, and the role played by them could explain why, in the case of some patients, Covid-19 targets several 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 checked for autoantibodies in 194 Covid-19 patients. They found that “Covid-19 patients exhibit dramatic increases in autoantibody reactivities” when compared to uninfected people in the study, and that these autoantibodies “target a wide range of immune-related proteins”. They also found, using a mouse model (tests on mice) that “immune-targeting antibodies exacerbate disease severity” and that the presence of autoantibodies that target “tissue-associated antigens” have a correlation with the severity of the disease.
Why is this important? One, it points (like all good studies do) to further avenues of research – in this case, the role of autoantibodies in the severity of Covid-19 infections. And two, it also points to possible therapies (or, at least, to the direction in which these may be found).
The second paper, titled “Post-infectious Inflammatory Disease in MIS-C features elevated cytotoxicity signatures and autoreactivity that correlates with severity”, is by Anjali Ramaswamy, Nina N Brodsky, Carrie L Lucas, and others. The researchers studied 15 children with MIS-C (multisystem inflammatory syndrome in children), an autoimmune disorder that can cause many body organs to become inflamed, and which is related 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 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 because of papers such as these two, we now know more about these than we previously did – can help identify and address MIS-C and other syndromes (initially, for instance, when the first cases of MIS-C emerged, doctors believed they were seeing manifestations of Kawasaki Disease). It also adds to what we know of long-Covid – which was among the first signs that, at least in some cases, Sars-CoV-2 has the same impact as autoimmune diseases.
We may have come up with vaccines that effectively prevent Covid-19, but we are still learning about the disease.