Severe COVID-19: We Have the culprit

When does Corona strike hard and when does it not? US researchers want to have found a main culprit for severe courses – on top of that, he could also be responsible for Long Covid.

The phenomenon of antibodies targeting the body’s own structures in COVID patients was observed early in the pandemic. Such Autoantibodies are suspected of having a special role in severe COVID-19 trends to play.

A working group led by Prof. Jean-Laurent Casanova from Rockefeller University in New York was one of the first to investigate the problematic immunoglobulins attentive. They found in seriously ill patients Autoantibodies especially against type I interferons. In the meantime, however, it has been shown that a whole range of different autoantibodies could arise as part of a COVID disease.

Dangerous immunoglobulins

For example, researchers at the University of Michigan had Autoantibodies against certain phospholipids prove can. That could explain why at Covid-19-Patients may experience problems with blood clotting – some of the phospholipids are involved in controlling hemostasis. Other US scientists had an increased prevalence of Autoantibodies against components of the Immune system in infected people compared to non-infected people found. Among other things, these were directed against B cells.

Based on the results of a recent Nature-Studie Scientists at Yale University headed by Aaron M. Ring are now even declaring autoantibodies to be the main culprit for a severe course.

The more autoantibodies, the more difficult the course

For their study, Ring et al. Blood samples from 194 COVID patients with varying degrees of severity to test for the presence of autoantibodies. In doing so, they used a new technology developed by Rings Laboratory called Rapid Extracellular Antigen Profiling (REAP) to identify autoantibody interactions with nearly 3,000 human proteins.

The more autoantibodies were detected, the more severe the degree of the disease in the patients. However, these autoantibodies were also found in test persons with slight progression.

They target the tissues or organs of a sick person and are similar to the autoantibodies that autoimmune diseases like Lupus or rheumatoide Arthritis cause. In the case of COVID-19, they can have healthy tissue in the brain, im Endothelium, the Plateletsattack the liver and gastrointestinal tract. At the same time, they also target many different proteins in the immune system, which disrupts the immune system. These proteins included those involved in the function and activation of lymphocytes, leukocyte trafficking, type I and type III interferon response, type II immunity, and the Acute phase response involved.

Autoimmune diseases due to infections

In many cases the presence of SARS-CoV-2 To promote the formation of harmful autoantibodies, the authors write in their study. Other scientists have already put forward this thesis: In one Study by Wang et al. had some of the infected people they studied Autoantibodies against proteins expressed in the endothelium, heart and brain. It was in these organs that people developed symptoms.

This phenomenon is not new. Autoantibodies can be induced not only by SARS-CoV-2, but also by infection with other pathogens. It is believed that infection increases the risk of autoimmune diseases. Apparently that seems immune system incorrectly classifying the body’s own proteins as foreign due to inflammation caused by an infection and Autoantibodies to form against these molecules.

On the other hand, according to the authors, it could also be that some COVID-19 patients already had autoantibodies that made them more susceptible to the infection. This is indicated by animal experiments carried out by Ring et al. performed: Mice with the same autoantibodies were more susceptible to infection with SARS-CoV-2 and were more likely to die.

Explanation for Long Covid?

The existence of these long-lived autoantibodies could also explain why some people infected with COVID-19 may later develop permanent medical symptoms – called long covid. However, this hypothesis has not yet been proven.

“Our results underline how important it is to get vaccinated,” adds immunologist and co-author Prof. Akiko Iwasaki added. “The fact that even mild infections are linked to the production of autoantibodies underscores the potential for long-term health consequences of COVID-19.”

Image source: Ronile, pixabay

Leave a Comment

This site uses Akismet to reduce spam. Learn how your comment data is processed.