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Some Covid-19 survivors bear troubling signs that their immune systems have activated on the body, reminiscent of potentially debilitating diseases like lupus and rheumatoid arthritis, a new study has found.
At some point, the body’s defense system in these patients switched to attacking itself, rather than the virus, the study suggests. Patients are producing molecules called “autoantibodies” that target genetic material from human cells rather than the virus.
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This misguided immune response can exacerbate severe COVID-19. It could also explain why so-called “long transporters” have persistent problems months after their initial illness clears up and the virus has disappeared from their bodies.
The findings have important implications for treatment: Using existing tests that can detect autoantibodies, doctors could identify patients who might benefit from treatments used for lupus and rheumatoid arthritis. There is no cure for these diseases, but some treatments reduce the frequency and severity of flare-ups.
“It’s possible you can hit the appropriate patients harder with some of these more aggressive drugs and expect better results,” said Matthew Woodruff, immunologist at Emory University in Atlanta and lead author of the work.
The results were reported on Friday on the MedRxiv prepress server and have not yet been published in a scientific journal. But other experts said the researchers who conducted the study are known for their careful and meticulous work, and that the results are not unexpected because other viral diseases also activate autoantibodies.
“I’m not surprised, but it’s interesting to see this really happening,” said Akiko Iwasaki, an immunologist at Yale University. “It is possible that even moderate to mild disease can induce this type of antibody response.”
For months it has been clear that coronavirus can drive the immune system crazy in some people, eventually causing more damage to the body than the virus itself. (Dexamethasone, the steroid that President Donald Trump took after his Covid diagnosis, has been shown to be effective in some people with severe Covid in suppressing this exuberant immune response.)
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Viral infections cause the death of infected human cells. Sometimes the cells die a quiet death, but sometimes, and especially in the throes of a serious infection, they can explode, scattering their entrails. When this happens, the DNA, normally enclosed in coiled bundles within the nucleus, is suddenly scattered and visible.
In the typical response to a virus, cells known as immune B cells make antibodies that recognize bits of viral RNA from the virus and lock onto them.
But in conditions like lupus, some B cells never learn to do this and instead produce autoantibodies that deposit on DNA debris from dead human cells, mistaking them for intruders. Something similar could happen in patients with Covid-19, the research suggests.
“Whenever you have that combination of inflammation and cell death, there’s the potential for autoimmune diseases and autoantibodies, more importantly, to emerge,” said Marion Pepper, an immunologist at the University of Washington in Seattle.
Woodruff and his colleagues reported earlier this month that some people with severe Covid-19 also have unrefined immune B cells. The discovery prompted them to explore whether those B cells produce autoantibodies.
In the new study, the researchers looked at 52 patients within the Emory Health System in Atlanta who had been classified as having severe or critical Covid-19 but who did not have a history of autoimmune diseases.
They found autoantibodies that recognize DNA in nearly half of the patients. They also found antibodies against a protein called rheumatoid factor and others that help with blood clotting. Among the top half of the most critically ill patients, more than 70 percent had autoantibodies against one of the targets tested, Woodruff said.
“It’s not just that these patients have an autoimmune immune response,” he said. “It’s that these immune responses are coupled with real testable clinical self-reactivity.”
Some of the autoantibodies the researchers identified are associated with blood flow problems, noted Ann Marshak-Rothstein, an immunologist and lupus expert at the University of Massachusetts, Worcester.
“It is very likely that some of the clotting problems you see in Covid-19 patients are driven by this type of immune complex,” he said.
If the autoantibodies prove to be long-lasting, he said, they can cause persistent, even lifelong problems for Covid-19 survivors.
“They never really cure lupus – they have flares, and they get better and they have flares again,” he said. “And that might have something to do with autoantibody memory.”
Marshak-Rothstein, Iwasaki, and dozens of other teams are closely studying the immune response to the coronavirus. Given the ease of testing for autoantibodies, it may soon become clear whether the antibodies were only identified because researchers went looking for them or if they represent a more permanent alteration of the immune system.
“It’s not clear to me what all of this means at this point,” Pepper said. “It will take some time to figure out if this is something that will lead to the downstream pathology.”
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