Patients with severe COVID-19 infections may produce antibodies that attack the body, similar to patients with chronic autoimmune disorders such as lupus and rheumatoid arthritis, an study posted on Oct. 23 by Emory researchers found.
The study, which is still a preprint awaiting peer review, identified forms of these antibodies, called autoantibodies, in 27 of 52 patients with severe COVID-19 infections. These autoantibodies are the result of a fumbled immune response in which B cells attack the body’s cells instead of the pathogen.
B cells produce antibodies, proteins that target specific pathogens. Typically, B cell immune responses “go through a really careful selection process” to ensure antibodies are calibrated to attack only the pathogen and not the body, according to Matthew Woodruff, immunologist at the Lowance Center for Human Immunology at Emory School of Medicine and lead author of the study.
Woodruff pointed out that this study merely provides evidence of nonstandard immune responses and signals only that autoantibody production may show up in many severe COVID-19 patients.
“We’ve documented that these responses are lupus-like; we’ve documented now that those lupus-like responses correlate with autoantibody production,” Woodruff said. “What that can’t tell you is whether those autoantibodies are directly contributing to disease pathology.”
Ignacio Sanz, director of the Lowance Center for Human Immunology and a co-author on the study, said one of the next questions that must be answered is whether this autoreactive response is contributing to the severity of the case or whether it is simply a byproduct.
The study also comes short of being able to show how long this effect lasts. A short-term autoimmune response to viral infection is not unheard of in other diseases.
“When you get mono, when you get rubella, when you get parvovirus [B19], things of that nature, it’s not unusual to have a transient autoimmune reaction,” Sanz said.
But these responses, as identified in patients in the study, have the potential to develop into long-term disease.
“I’m sure it’s going to be different from patient to patient,” Sanz added.
If further studies show that COVID-19 infection can result in chronic autoimmune disorders, doctors may have a route to treat the autoimmune response that is not typically available because there is still time to counter the disease.
“In normal situations, when we see a patient with lupus or a patient with rheumatoid arthritis, even if they are diagnosed today for the first time, we know that the disease has been going on for at least 10 years before it manifests itself clinically,” Sanz said. “And so, in a way, the window of time to do preemptive treatment or early treatment [is] almost gone because the autoimmune disorder has been going on for quite some time.”
However, Sanz also pointed out that this would present a problem in treating COVID-19 itself. While the immunosuppressants could prevent a harmful immune response, they would also impair the body’s ability to fight the virus.
“It’s an issue of balance in the individual patient,” Sanz said.
For Woodruff, the finding indicates a chance to learn about the initial development of autoimmune diseases, which is difficult to study because of the time lapse between the beginnings of the conditions and the appearance of symptoms.
“I think that we find ourselves in a position where we can really do some good by really understanding the initial phases of what these kinds of responses look like,” he noted.