Autoantibodies directed against interferon alpha, nuclear antigens, cardiolipin, and beta 2 glycoprotein 1 are not induced by SARS-CoV-2 or associated with long COVID

• Published in: International journal of infectious diseases 2025-01, Vol.150, p.107289, Article 107289
• Main Authors: Epstein-Shuman, Adam, Hunt, Joanne H., Caturegli, Patrizio, Winguth, Patrick, Fernandez, Reinaldo E., Rozek, Gracie M., Zhu, Xianming, DiRico, Nicholas A., Jamal, Armaan, Hsieh, Yu-Hsiang, Manabe, Yukari C., Redd, Andrew D., Reynolds, Steven J., Antar, Annukka A.R., Laeyendecker, Oliver
• Format: Article
• Language: English
• Subjects: Adult; Aged; Autoantibodies; Autoantibodies - blood; Autoantibodies - immunology; beta 2-Glycoprotein I - immunology; Cardiolipins - immunology; COVID-19; COVID-19 - immunology; Female; Humans; Interferon-alpha - blood; Interferon-alpha - immunology; Long COVID; Male; Middle Aged; Post-Acute COVID-19 Syndrome; SARS-CoV-2; SARS-CoV-2 - immunology
• ISSN: 1201-9712; 1878-3511; 1878-3511
• DOI: 10.1016/j.ijid.2024.107289

•COVID-19 severity has been associated with the presence of autoantibodies.•Autoantibodies aIFNα, ANA, aCL, & aβ2GP1 were not induced by SARS-CoV-2 infection.•Observed autoantibody prevalence was the same in those with and without long COVID. Autoantibodies (AAbs) directed against interferon alpha (aIFNα), nuclear antigens (ANAs), anti-cardiolipin (aCL), and anti-beta 2 glycoprotein 1 (aβ2GP1), have been demonstrated to significantly correlate with the severity of acute Coronavirus Disease 2019 (COVID-19). However, whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection induces these AAbs and whether they are associated with long COVID remains unclear. The potential induction of aIFNα, ANAs, aCL, and aβ2GP1 by SARS-CoV-2 was assessed by measuring these AAbs in 224 pre- and post-infection paired serum samples from the Johns Hopkins Hospital Emergency Department (JHHED). The relationship between these AAbs and long COVID was assessed using 60 serum samples from participants in the Outpatient SARS-CoV-2 Mild and Asymptomatic Infection Response and Transmission study. We found no evidence that these AAbs were induced in the JHHED cohort and no significant difference in their prevalence between patients with (n = 30) and without (n = 30) long COVID in the OutSMART cohort. These findings do not support the hypotheses that SARS-CoV-2 induces these AAbs or that they are related to long COVID.