How the Coronavirus Turns the Body Against Itself – The New York Times

One in five infected patients had autoantibodies to five proteins in their own bodies, and up to 80 percent to at least one protein, the researchers found. Patients with severe Covid-19 had many more of these antibodies, which hindered their immune responses and exacerbated illness. Of 15 patients who died during the study, 14 had autoantibodies to at least one constituent of the immune system.

The study convincingly shows that autoantibodies “alter the course of disease,” said Marion Pepper, an immunologist at the University of Washington in Seattle who was not involved in the research.

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Autoimmunity after an illness is not unique to the coronavirus. Other intensely inflammatory infections, including malaria, leprosy and respiratory viruses, are also known to trigger autoantibodies. But autoimmunity and Covid-19 may be a particularly hazardous mix, experts said.

One analysis of nearly 170,000 people with rare autoimmune rheumatic diseases like lupus and scleroderma indicated that they face increased odds of death from Covid-19. And a study of more than 130,000 people found that autoimmune conditions like Type 1 diabetes, psoriasis and rheumatoid arthritis increase the risk of respiratory complications and death from Covid-19.

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Some of the antibodies seemed to be the result of inborn defects in the immune system. For example, a study in the journal Science in October found that about 10 percent of severely ill Covid-19 patients had existing autoantibodies that attacked key components of the immune system that were supposed to kick in after exposure to the virus. Without that rapid response, the body’s defense is hopelessly delayed, fighting a losing battle against the multiplying virus.

Yet the mere presence of autoantibodies does not indicate harm. They are in the general population and don’t always lead to illness, some experts noted.

“Anywhere from 10 to 15 percent of the population has some level of this auto-reactivity,” said Dr. Iñaki Sanz, an immunologist at Emory University. “The issue is that you need many other events downstream of the autoantibodies to induce disease.”

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