A new study found that some survivors of Covid-19 have worrying signs that their immune systems have turned on their bodies, reminiscent of debilitating diseases such as lupus and rheumatoid arthritis.
The study showed that at some point, these patients’ body defense systems began to attack themselves instead of viruses. Patients are producing molecules called “autoantibodies” that target the genetic material of human cells rather than viruses.
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These findings have important implications for treatment: Using existing tests that can detect autoantibodies, doctors can identify patients who may benefit from treatment for lupus and rheumatoid arthritis. There is no cure for these diseases, but certain treatments can reduce the frequency and severity of attacks.
The lead author of the paper, immunologist Matthew Woodruff of Emory University in Atlanta, said: “Using these more aggressive drugs may make you hit the right patients harder and expect better results. .”
The results were reported on the preprint server MedRxiv on Friday and have not yet been published in a scientific journal. But other experts say that the researchers who conducted this study are known for their meticulous and meticulous work, and found that the results are not unexpected, because other viral diseases also trigger autoantibodies.
Yale University immunologist Akaki Iwasaki said: “I’m not surprised, but it is interesting that it is happening.” “Even moderate to mild disease may induce this antibody response.”
For several months, it has become clear that the coronavirus can make some people’s immune system function abnormally, and ultimately cause more damage to the human body than the virus itself. (Dexamethasone taken by President Donald Trump after receiving a Covid diagnosis has been shown to be effective in reducing this excessively exuberant immune response for some people with severe Covid.)
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Viral infection causes the death of infected human cells. Sometimes these cells die quietly-but sometimes, especially in the pain of a severe infection, they may explode and spread internal organs. When this happens, the DNA that is usually gathered in a spiral bundle in the nuclear bundle will suddenly spread out and become visible.
In a typical response to a virus, cells called B immune cells produce antibodies that recognize and lock onto the viral RNA fragments in the virus.
But in the case of lupus, some B cells will never learn to do this. Instead, they will produce auto-antibodies, which will condense from dead human cells to DNA fragments, making them mistakenly believe they are invaders. Research shows that a similar situation may occur in Covid-19 patients.
Marion Pepper, an immunologist at the University of Washington in Seattle, said: “Whenever inflammation and cell death coexist, autoimmune diseases and autoantibodies are more likely to occur.”
Woodruff and his colleagues reported earlier this month that some people with severe Covid-19 also have such unrefined B immune cells. This discovery prompted them to explore whether those B cells produced autoantibodies.
In this new study, researchers studied 52 severe or severe Covid-19 patients in the Emory health care system in Atlanta, but no history of autoimmune diseases.
They found autoantibodies that recognize DNA in nearly half of patients. They also discovered antibodies against rheumatoid factor protein and other antibodies that help blood clotting. Woodruff said that in the upper half of the most severely ill patients, more than 70% of patients have autoantibodies against a tested target.
He said: “It is not just these patients who have autoimmune-like immune responses.” “It is these immune responses that are combined with actual testable clinical autoreactivity.”
Ann Marshak-Rothstein, an immunologist and lupus expert at the University of Massachusetts in Worcester, pointed out that some of the autoantibodies discovered by the researchers are related to blood flow problems.
She said: “Some of the coagulation problems seen in Covid-19 patients are likely to be driven by this type of immune complex.”
She said that if autoantibodies are indeed persistent, they may cause persistent or even lifelong problems for Covid-19 survivors.
She said: “You have never really cured lupus-they have flares, they will get better, and there will be flares.” “This may be related to autoantibody memory.”
Marshak-Rothstein, Iwasaki and dozens of other groups are closely studying the immune response to the coronavirus. Given the simplicity of autoantibody testing, it will soon be possible to figure out whether antibodies were identified only because researchers have been searching for antibodies, or whether they represent more permanent changes in the immune system.
“I don’t know what this means,” Pepper said. “It will take a while to figure out whether this will cause downstream pathology.”