On his computer, Ring can pull up several graphs displaying the population of 15 different autoantibodies found in several patients as their infection progressed. Just as Casanova described, antibodies against interferon are clearly visible in the blood when patients were first tested at the hospital. Those numbers stay high as the infection progresses. But Ring found the trajectory to be quite different for the other autoantibodies.
In the initial samples, autoantibodies except for the ones against interferon are nonexistent or undetectable in the blood. Those other antibodies first appear in subsequent blood samples and continue to rise as the infection persists. It seemed to confirm Ring’s worst fears: that those autoantibodies were created by covid itself.
“These are very clearly newly acquired—no question about it,” he explains, pointing to one line of rising autoantibodies. “They came up during the course of infection. The infection triggered autoimmunity.”
In most of those patients, the autoantibodies returned to undetectable levels in subsequent blood samples. But in some, the autoantibodies remained high at the point of last testing—in some cases more than two months after infection. Some of those patients developed long covid.
“We have been, publicly and in the paper, pretty cautious about the interpretation of our results,” he says. “But this does have implications for post-covid syndrome, because autoantibodies can plausibly persist well after the virus has been dealt with.”
An all-out attack
Why do these new autoantibodies appear? Some enticing clues have emerged. In October, a team of researchers led by Ignacio Sanz, an expert on lupus at Emory University, documented a phenomenon in the immune system of many severe covid patients that is often seen during lupus flare-ups.
It occurs in the specialized immune cells known as B cells, which produce antibodies. In order to quickly scale up production of the B cells needed to combat the covid virus, Sanz explains, the immune systems of some patients seem to take a dangerous shortcut in the biological process that usually determines which antibodies the body generates to fight off a specific infection.