Researchers pinpoint autoimmune antibodies that may predict COVID-19 severity

Throughout the pandemic, researchers have determined that the eventual immune response to COVID-19 can do more damage than the initial respirator-related reactions the virus triggers. Now a new study has pinpointed specific antibodies that are associated with some of that damage, potentially providing hospitals with insight to determine how best to treat patients admitted with COVID-19.

Researchers at New York University's Grossman School of Medicine discovered that autoimmune antibodies that bind to DNA or the fat molecule phosphatidylserine appear to be the bad actors in COVID-19. These antibodies were twice as abundant at the start of a COVID-19 infection in patients whose conditions worsened quickly compared to those who didn't experience a decline in health, the team reported in the journal Life Science Alliance.

The autoimmune antibodies attacked the patients' healthy cells, making those with higher levels of these antibodies five to seven times more likely to have severe cases of COVID-19 when compared to patients with stable levels, the NYU researchers found. Patients with high levels of the autoantibodies were more likely to need intensive care and mechanical ventilators than those with lower levels, who usually were able to breathe on their own. 

Testing for the presence of the autoimmune antibodies could help hospitals determine which patients need the most intensive care and monitoring, the researchers said. That could be critical insight, as the delta variant of the virus roils through the country, filling up hospitals and leaving healthcare professionals struggling to care for patients. 

The researchers retroactively examined the medical records and blood tests of 115 people hospitalized for COVID-19 from April to June 2020 at NYU Langone and found autoimmune antibodies in 36% of them. Of those patients, 93% had antiphosphatidylserine antibodies and 86% had anti-DNA antibodies. The production of those autoimmune antibodies correlated with blood clotting and cell death in patients with severe cases of COVID-19, the researchers said.

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Finding new ways to ameliorate the overactive immune response seen in COVID-19 patients has been a major focus of research since the start of the pandemic. Last year, a Johns Hopkins team showed how inhibiting factor D could prevent the spike protein on SARS-CoV-2, the virus that causes COVID-19, from activating a dangerous chain of immune reactions to the illness. More recently, scientists at the Indian Council of Medical Research said a century-old tuberculosis vaccine could potentially fight COVID-19 by promoting an immune response that could tamp down inflammatory cytokines. 

The NYU team cautioned that more information needs to be gathered to understand whether the autoimmune antibodies they zeroed in on are the cause or effect of dangerous clotting in severe COVID-19. 

If the antibodies are the cause, then the findings could be useful for developing new COVID-19 treatments, they said. For example, antibody injections from healthy donors could help mitigate the autoimmune antibodies. Another option would be to develop biodegradable antigens that can neutralize the autoimmune antibodies without causing an immune reaction, they added.