{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T22:35:19Z","timestamp":1790030119300,"version":"4.0.1"},"reference-count":19,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2023,7,7]],"date-time":"2023-07-07T00:00:00Z","timestamp":1688688000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Med."],"abstract":"<jats:sec><jats:title>Objectives<\/jats:title><jats:p>To investigate the association between severe acute respiratory syndrome-associated coronavirus-2 (SARS-CoV-2) infection and subsequent development of autoimmunity or pre-clinical manifestations associated with rheumatoid arthritis (RA) in at risk population.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>This is a nested study within a prospective cohort of first-degree relatives of RA patients (RA-FDR). Participants are tested for RA-associated autoantibodies (anti-citrullinated peptide antibodies (ACPA)\/rheumatoid factor (RF)) and clinical signs and symptoms suggestive of early disease. SARS-CoV-2 infections were self-reported between March 2020 and January 2023. All individuals with a pre-pandemic (sample 1) and a post-pandemic sample (sample 2) were included in the analysis. The exposure of interest was self-reported SARS-CoV-2 infection. The primary outcome was a clinically significant change in RA-associated autoantibody serum titers. Secondary outcomes included: becoming seropositive, becoming symptomatic, developing classifiable RA.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Among 168 RA-FDRs, 109 reported a SARS-CoV-2 infection between sample 1 and sample 2. During this period, 2 RA-FDRs (1.2%) became anti-CCP2 seropositive, none became anti-CCP3 IgG positive, 6 (3.6%) became RF IgM seropositive, 1 became (0.6%) RF IgA seropositive, 19 (11.3%) became symptomatic and none developed classifiable RA. SARS-CoV-2 infection was not significantly associated with increases in RA autoantibody titers or with secondary outcomes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>We could not detect an association between SARS-CoV-2 infection and subsequent development of RA-associated autoimmunity, nor signs or symptoms of RA in an at risk population. These findings do not support the hypothesis that SARS-CoV-2 infections triggers the immune onset of RA.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fmed.2023.1201425","type":"journal-article","created":{"date-parts":[[2023,7,7]],"date-time":"2023-07-07T16:18:27Z","timestamp":1688746707000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":10,"title":["Brief report: can COVID-19 infection trigger rheumatoid arthritis-associated autoimmunity in individuals at risk for the disease? A nested cohort study"],"prefix":"10.3389","volume":"10","author":[{"given":"Celine","family":"Lamacchia","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benoit","family":"Gilbert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivia","family":"Studer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kim","family":"Lauper","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Axel","family":"Finckh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2023,7,7]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","first-page":"102792","DOI":"10.1016\/j.autrev.2021.102792","article-title":"The SARS-CoV-2 as an instrumental trigger of 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