Scientists from Yale University, which carried out the study, observed Covid patients with these misguided proteins that attacked healthy organs and the person’s own immune system instead of battling against the virus.
The immune systems of some Covid-19 patients may be turning against their own bodies, triggering complications including “long Covid”, scientists have found.
So-called autoantibodies in people infected with coronavirus could be interfering with their immune response, contributing to more severe cases of the disease in some patients and leaving others suffering from the effects of the virus months later.
The more autoantibodies a patient had in their blood, the worse they seemed to be affected by the disease.
Aaron Ring, an immunobiologist at Yale and senior author on the study, told The Guardian: “Covid-19 patients make autoantibodies that actually interfere with immune responses against the virus.
“We certainly believe that these autoantibodies are harmful to patients with Covid-19.
“Because antibodies can persist for a long time, it’s conceivable that they may contribute to the development of long-Covid diseases.”
Antibodies are proteins produced by the immune system to help the body to recognise and fight infection. Autoantibodies are antibodies that recognise and fight healthy parts of the body instead of invading viruses.
The researchers worked with 194 Covid patients and healthcare workers to study 2,770 proteins.
Akiko Iwasaki, a professor of immunobiology at Yale who co-authored the report, said: “Our findings provide clues for why Covid affects many organs [and] induce [a] range of symptoms that are long lasting.
“A large fraction of Covid patients had autoantibodies to multiple self antigens. The more severe the disease, [the] more autoantibodies they had.”
But she added: “There are many unanswered questions. How long do these autoantibodies last? What damage do they cause? How are they induced? Do they occur in long Covid?”
The study has not yet been peer reviewed or published in a journal.