RA and SLE-related Autoreactivities Present in Those with COVID-19

September 26, 2022

A recent study was published as an accelerated article preview addressing the origin of autoantibodies by looking at patients with acute infection of SARS-CoV-2. 

Autoantibodies are a key characteristic of COVID-19 triggered autoimmunity, when B-cells self-direct instead of attacking foreign invaders (SARS-CoV-2 cells). At the time of the study, “evidence of autoreactivity was mounting in severe disease, with observations of autoantibody-linked blood clotting, anti-interferon antibodies, connective tissue disease-associated interstitial lung disease, and generalized observations of clinical autoreactivity.” Within the study, anti-nuclear antigens (ANA) and anti-carbmamylated protein responses (CarP) were found in over 40% of the 27 ICU patients with COVID-19. These antibodies are also associated with tissue damage in RA and SLE. When compared to ICU patients hospitalized with bacterial pneumonia, auto-reactivity profiles were “highly similar… strongly suggesting that the autoimmune phenomena described in COVID-19 to-date may be generalizable to other severe pulmonary infections.” 

Autoimmunity is considered to be a mechanism of long Covid. Researchers found that approximately one third of patients with long Covid had elevated levels of autoantibodies for months post initial-infection. For most COVID-19 patients, autoantibodies rid themself from the body after the acute infection phase is resolved. However, those with long Covid continued to circulate autoantibodies. 

What has yet to be studied is whether these autoantibodies are directly contributing to long Covid symptoms, and whether certain therapies can decrease autoantibody counts to thereby decrease symptoms. Researchers also hope to address the development of autoantibodies in regard to viral infections more broadly.





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