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Immune systems of COVID-19 patients may attack their own bodies

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Immunologists are trying to explain why some people get so sick while others recover without major consequences. New data revealed by a group of scientists suggest that the key could be in our organisms’ autoimmune response.

One area of ​​special interest to scientists has been the production of antibodies, powerful proteins capable of disabling and killing invading pathogens, such as viruses. Scientists pay particular attention to the sporadic identification of autoreactive antibodies that, instead of fighting disease-causing microbes, target the tissues of individuals suffering from severe cases of COVID-19.

The first studies relate these autoantibodies, that is, the antibodies developed by the immune system that act against one or more antigens of the individual, with the dangerous blood clots that form in patients admitted to intensive care. Lately, they have been related to a serious disease since they inactivate important components of viral defenses in a large part of patients.

An autoimmune response to COVID

Immunologist Lowance Center for Human Immunology at Emory University, Matthew Woodruff, investigated the immune response responsible for producing antibodies in COVID-19. Under the direction of Dr. Ignacio Sanz, his group previously studied the immune responses that contribute to the production of autoantibodies in autoimmune disorders such as lupus, as well as in severe cases of COVID-19.

Researchers were able to characterize the response in COVID-19 patients as autoimmune, but were unable to confirm the production of hidden autoantibodies within their antiviral responses.

But now, in a newly published study, scientists describe that in patients with the most severe cases of COVID-19, autoantibody production is common. In other words, severe infection is related to the production of autoantibodies.

Autoantibodies are generally associated with specific types of diseases. Lupus patients, for example, often have antibodies that target their own DNA; those with the autoimmune disorder rheumatoid arthritis are less likely to have those antibodies.

In this study, the group from the Lowance Center for Human Immunology analyzed the medical records of 52 patients with severe cases of COVID-19. None of them had a history of autoimmune disorders before. However, these antibody disorders were found after they got sick.

More than half of the 52 patients had autoantibodies. In individuals with the highest levels of C-reactive protein in their blood, more than two-thirds showed evidence that their immune systems were producing antibodies that attacked their own tissue.

The unknowns persist

However, there are things that the collected data does not reveal. The extent to which these autoantibodies contribute to the most severe symptoms of COVID-19 is not yet known. It could be that a serious viral illness consisted of the production of autoantibodies with little consequence. We also do not know how long autoantibodies last. The data suggest that they are relatively stable for a few weeks.

While it is possible that these autoantibodies are benign or even helpful in an as-yet-unidentified way, it is also likely that they are not, the study authors note. Perhaps these self-directed antibody responses contribute to the severity of the disease, helping to explain the delayed onset of severe symptoms in some patients that may be related to antibody production.

These responses may not be short-lived, outpacing the infection and contributing to the ongoing symptoms now experienced by large numbers of COVID-19 patients. Most worryingly, these responses could be self-perpetuating in some patients, leading to new permanent autoimmune disorders. Matthew Woodruff and his colleagues hope that this is not the case, but rather that the appearance of autoantibodies in these patients is a quirk of the viral immune response.

This study shows that these two autoantibodies and the inflammatory marker C-reactive protein can identify patients who are more likely to experience potentially dangerous immune responses that could benefit from a more aggressive modulation of the immune response.

The scientists conclude that after examining patients after their recovery from COVID-19, baselines can be established and can begin to investigate the possible appearance of new cases of autoimmunity after suffering from this disease. Currently for these studies there are all the tools, they say. 

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