COVID-19 associated autoimmunity is a feature of severe respiratory disease - a Bayesian analysis

Abstract

Background: Serological and clinical features with similarities to systemic autoimmunity have been reported in severe COVID-19, but there is a lack of studies that include contemporaneous controls who do not have COVID-19. Methods: Observational cohort study of adult patients admitted to an intensive care unit with acute respiratory failure. Patients were divided into COVID+ and COVID- based on SARS-CoV-2 PCR from nasopharyngeal swabs and/or endotracheal aspirates. No COVID-19 specific interventions were given. The primary clinical outcome was death in the ICU within 3 months; secondary outcomes included in-hospital death and disease severity measures. Measurements including autoantibodies, were done longitudinally. ANOVA and Fisher's exact test were used with alpha=0.05, with a false discovery rate of q=0.05. Bayesian analysis was performed to provide credible estimates of the possible states of nature compatible with our results. Results: 22 COVID+ and 20 COVID- patients were recruited, 69% males, median age 60.5 years. Overall, 64% had anti-nuclear antibodies, 38% had antigen-specific autoantibodies, 31% had myositis related autoantibodies, and 38% had high levels of anti-cytokine autoantibodies. There were no statistically significant differences between COVID+ and COVID- for any of the clinical or autoantibody parameters. A specific pattern of anti-nuclear antibodies was associated with worse clinical severity for both cohorts. Conclusions: Severe COVID+ patients have similar humoral autoimmune features as comparably ill COVID- patients, suggesting that autoantibodies are a feature of critical illness regardless of COVID-19 status. The clinical significance of autoimmune serology and the correlation with severity in critical illness remains to be elucidated.

Factors associated with immune responses to SARS-CoV-2 vaccination in autoimmune disease individuals

“…Autoantibodies to cardiolipin are induced by SARS-CoV-2 infection, and there was a significant incidence of thrombosis in subjects infected during the initial waves of the pandemic (30)(31)(32)(33).…”