Some COVID survivors have antibodies that attack the body, not the...

Some COVID survivors have antibodies that attack the body, not the...
Some COVID survivors have antibodies that attack the body, not the...
By: New York Times |

Updated: October 28, 2020, 9:54:38 am





Some COVID-19 survivors have had worrying signs that their immune systems have turned their bodies on, reminiscent of potentially debilitating diseases like lupus and rheumatoid arthritis. This is what a new study found. (Representative image)

Some COVID-19 survivors have had worrying signs that their immune systems have turned their bodies on, reminiscent of potentially debilitating diseases like lupus and rheumatoid arthritis. This is what a new study found.

At some point, the body’s defense system shifted to itself rather than the virus in these patients, the study said. Patients produce molecules called “autoantibodies” that target genetic material from human cells instead of the virus.

This misdirected immune response can make severe COVID-19 worse. This could also explain why so-called “long distance riders” have persistent problems months after their initial illness has ended and the virus has passed from their bodies.

The results have important implications for treatment: Existing tests to detect autoantibodies could help doctors identify patients who could benefit from treatments for lupus and rheumatoid arthritis. There is no cure for these diseases, but some treatments reduce the frequency and severity of flare-ups.

“It is possible that with some of these more aggressive drugs, you might hit the patient harder and expect better results,” said Matthew Woodruff, an immunologist at Emory University in Atlanta and lead author on the paper.

The results were published on Friday on the preprint server MedRxiv and have not yet been published in a scientific journal. However, other experts said the researchers who conducted the study are known for their meticulous and painstaking work, and that the results are not unexpected as other viral diseases also trigger autoantibodies.

“I’m not surprised, but it’s interesting to see it really happen,” said Akiko Iwasaki, an immunologist at Yale University. “It is possible that even moderate to mild illnesses trigger this type of antibody response.”

For months it has been clear that the coronavirus can cause the immune system to run amok in some people, which ultimately does more damage to the body than the virus itself. (Dexamethasone, which the steroid president Donald took after his COVID diagnosis shown to be effective in curbing this excessive immune response in some people with severe COVID.)

Virus infections lead to the death of infected human cells. Sometimes the cells die a silent death – but sometimes, and especially during times of severe infection, they can explode and spread their innards. When this happens, DNA, which is usually gathered in coiled bundles in the core, suddenly becomes scattered and visible.

In the typical response to a virus, cells known as B immune cells make antibodies that recognize pieces of viral RNA from the virus and bind to them.

But in conditions like lupus, some B cells never learn this and instead produce autoantibodies that stick to the DNA debris from dead human cells, mistaking them for intruders. Something similar could happen to patients with COVID-19, according to research.

“Any time you have this combination of inflammation and cell death, autoimmune diseases and autoantibodies can potentially occur,” 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 such unrefined B immune cells. The findings prompted them to investigate whether these B cells produce autoantibodies.

In the new study, researchers looked at 52 patients in the Emory health system in Atlanta who were rated either severe or critical but had no prior history of autoimmune diseases.

They found autoantibodies that recognize DNA in almost half of the patients. They also found antibodies to a protein called rheumatoid factor and others that help blood clot. Among the top half of the most severely ill patients, more than 70% had autoantibodies against any of the targets tested, Woodruff said.

“It’s not just that these patients have an autoimmune-like immune response,” he said. “The fact is that these immune responses are coupled with actually testable clinical auto-reactivities.”

Some of the autoantibodies identified by the researchers are linked to 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 that occur in COVID-19 patients are caused by these types of immune complexes,” she said.

If the autoantibodies are found to be long-lived, they could lead to persistent, even lifelong problems for COVID-19 survivors.

“You never really cure lupus – they have flares and they get better and they have flares again,” she said. “And that may have something to do with autoantibody storage.”

Marshak-Rothstein, Iwasaki, and dozens of other teams are closely examining the immune response to the coronavirus. With the ease of testing for autoantibodies, it may soon become clear whether the antibodies were only identified because the researchers were looking for them or whether they represent a more permanent change in the immune system.

“I’m not sure what this all means at this point,” said Pepper. “It will take a little time to understand if this will lead to downstream pathology.”

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