Stunning new research from the Emory Healthcare system in Atlanta found that certain survivors of COVID-19 develop an autoimmune response in which the body creates “autoantibodies” that attack human cells rather than the virus.

The researchers compared the mechanism to lupus or rheumatoid arthritis, conditions that are not curable, but treatable. Autoantibodies may explain why some COVID-19 patients become “long-haulers,” suffering from long-term symptoms after the initial infection.

According to The New York Times, medical experts have long witnessed the devastation the virus can have on the entire body when the immune response goes into overdrive. The steroid drug, dexamethasone, which was given to President Donald Trump, helps keep that overreaction under control.

Under normal circumstances, the body’s B immune cells make antibodies that attack an invading virus. B cells, also called B lymphocytes, are white blood cells that fight off infections from bacteria and viruses and help create antibodies that remember the attacker, according to Verywell Health.

But in some people, such as those who suffer from lupus, the B cells create autoantibodies that erroneously attack their own DNA on the cells killed by the virus, and not the enemy itself. The Emory scientists theorize that this may also be happening to COVID-19 patients.

“Anytime you have that combination of inflammation and cell death, there is the potential for autoimmune disease and autoantibodies, more importantly, to emerge,” Dr. Marion Pepper, associate professor of immunology at the University of Washington, told the Times.

Dr. Matthew Woodruff and his team, who conducted the new research, found that nearly half of the severely ill COVID-19 patients tested had autoantibodies that recognized DNA. His discovery could lead to new treatments that could reduce flareups.

“It’s possible that you can hit the appropriate patients harder with some of the more aggressive drugs and expect better outcomes,” said Woodruff, an immunologist at Emory University.