Differences in SARS-CoV-2 antigen persistence in individuals with systemic autoimmune rheumatic diseases compared to the general population: A RECOVER-Adult Cohort Study.

Patel, Naomi J; Swank, Zoe; Wang, Jiaqi; Wang, Xiaosong; O'Keeffe, Lauren A; Negron, Madison; Getachew, Liya S; Hansen, Louise L et al. · Arthritis Rheumatol · 2026

retrospective_cohort · Level III

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Abstract

Individuals with systemic autoimmune rheumatic diseases (SARDs) are at risk for worse acute and post-acute COVID-19 outcomes, though whether individuals with SARDs have longer persistence of viral antigens after COVID-19 has not been studied. This retrospective cohort study evaluated post-COVID-19 differences in SARS-CoV-2 antigen (spike, S1, and nucleocapsid) positivity between individuals with SARDs (RheumCARD) and without SARDs (RECOVER-Adult). SARS-CoV-2 antigens were measured in collected samples using a validated ultra-sensitive single molecule array. This digital enzyme-linked immunosorbent assay used antibody-coated magnetic beads to capture antigen molecules, which were loaded into microwell arrays and detected through enzymatic cleavage of a fluorescent substrate. We used logistic regression to estimate unadjusted and adjusted (for age, sex, infection year, vaccination status, and COVID-19 treatment) odds ratios for SARS-CoV-2 antigen positivity at months 3 and 6 following COVID-19. Among 210 individuals with SARDs in RheumCARD and 348 individuals without SARDs in RECOVER-Adult, any SARS-CoV-2 antigen positivity was more common in those with SARDs (36.7% in RheumCARD vs. 18.9% in RECOVER-Adult; p<0.001). Those with SARDs had higher odds of nucleocapsid antigen positivity (adjusted OR 3.73, 95% CI: 1.28-10.85) or any antigen positivity (adjusted OR 2.89, 95% CI: 1.43-5.85) 3 months after COVID-19 infection and higher odds of nucleocapsid antigen positivity (adjusted OR 6.62, 95% CI: 1.09-40.30) 6 months after COVID-19 infection. Individuals with SARDs were more likely to have SARS-CoV-2 antigen positivity at months 3 and 6 following COVID-19 infection compared with individuals without SARDs, not explained by demographics, variant, vaccination, or treatment.