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Some Covid-19 survivors have worrying signs that their immune system has been activated in the body, reminiscent of potentially debilitating diseases like lupus and rheumatoid arthritis, a new study found.
Sometime, The body’s defense system in these patients changed to attack itself, rather than the virus, the study suggests. Patients are producing molecules called “autoantibodies” that target the genetic material of human cells, rather than the virus.
This wrong immune response can exacerbate severe Covid-19. It can also explain why so-called “long-haul carriers” have persistent problems months after their initial illness has resolved and the virus has cleared 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 the treatments used for lupus and rheumatoid arthritis. There is no cure for these diseases, but some treatments decrease the frequency and severity of flare-ups.
“You may be able to hit the appropriate patients harder with some of these more aggressive drugs and expect better results,” said Matthew Woodruff, an immunologist at Emory University in Atlanta and lead author on the paper.
The results were reported Friday on the MedRxiv prepress server and have yet to be 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 findings are not unexpected because other viral diseases also trigger autoantibodies.
“I’m not surprised, but it’s interesting to see what is 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 the coronavirus can cause the immune system to go haywire in some people, ultimately causing more damage to the body than the virus itself. (Dexamethasone, the steroid President Trump took after his Covid diagnosis, has been shown to be effective in some people with severe Covid at suppressing this exuberant immune response.)
Viral infections cause the death of infected human cells. Sometimes the cells die silently, but sometimes, and especially in the midst of a serious infection, they can burst and seed your guts. When that happens, the DNA, normally cloistered in bundles coiled within the nucleus, is scattered and suddenly seen.
In the typical response to a virus, cells known as immune B cells produce antibodies that recognize and bind to viral RNA fragments of the virus.
But in conditions like lupus, some B cells never learn to do this and instead produce autoantibodies that stick to the DNA debris of dead human cells, mistaking them for intruders. Something similar may be happening in Covid-19 patients, the research suggests.
“Every time that combination of inflammation and cell death occurs, there is the potential for autoimmune diseases and autoantibodies to emerge, most importantly,” said Marion Pepper, an immunologist at the University of Washington in Seattle.
Dr. Woodruff and his colleagues reported earlier this month that some people with severe Covid-19 also have unrefined B immune cells. The finding led them to explore whether those B cells produce autoantibodies.
In the new study, researchers looked at 52 patients within Emory’s health care system in Atlanta who were classified as severe or critical Covid-19, but who had no history of autoimmune disorders.
They found autoantibodies that recognize DNA in almost 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 severely ill patients, more than 70 percent had autoantibodies against one of the targets tested, Dr. Woodruff said.
“It’s not just that these patients have an autoimmune-type immune response,” he said. “It’s that these immune responses are combined with real and verifiable clinical self-reactivities.”
Some of the autoantibodies the researchers identified are associated with blood flow problems, said Ann Marshak-Rothstein, an immunologist and lupus expert at the University of Massachusetts, Worcester.
“It is very possible that some of the clotting problems seen in Covid-19 patients are driven by these types of immune complexes,” he said.
If the autoantibodies turn out to be long-lasting, he said, they can result in lingering, even lifelong problems for Covid-19 survivors.
“Lupus is never really cured; they have sprouts, they get better and sprout again, ”he said. “And that may have something to do with autoantibody memory.”
Dr. Marshak-Rothstein, Dr. Iwasaki, and dozens of other teams are closely studying the immune response to the coronavirus. Given the ease of autoantibody testing, it will soon become clear whether the antibodies were identified just because researchers went looking for them or whether they represent a more permanent alteration of the immune system.
“I’m not clear about what all of this means at this point,” Dr. Pepper said. “It’s going to take a bit of time to understand if this is something that’s going to lead to further pathology.”
