Researchers have determined that the severe course of COVID-19 is due to an autoimmune reaction, during which immune cells attack the body itself. In contrast to the overactive inflammatory response seen in cytokine storms, autoantibodies promote targeted, long-term damage. This is reported in an article published in the journal Nature.
Autoantibodies were discovered back in September 2020 by a group of scientists from Rockefeller University in more than 10 percent of nearly a thousand people with severe COVID-19. The antibodies mainly attacked and blocked the action of the type I interferon molecules that mediate the immune response. People in the control group did not have autoantibodies.
Researchers believe that some people may be genetically predisposed to produce antibodies, with these molecules being observed more often in men, which may explain why men are more susceptible to coronavirus than women.
Currently, scientists are examining 40 thousand people for the presence of autoantibodies and their connection with severe coronavirus infection. According to as yet unpublished data, the high prevalence of autoantibodies directed against the immune system is more common in infected people than in uninfected people. Autoantibodies have been identified that attack B cells, as well as some that attack interferon. A number of those infected had autoantibodies to proteins in the blood vessels, heart and brain.
Another group of researchers found that deceased people have a significantly higher average level of antibodies to annexin A2 than people with non-critical illness. Thus, autoimmunity could be the real cause of deadly organ destruction that continues even after the coronavirus itself has disappeared.