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Autoantibodies to interferon alpha, nuclear antigens, cardiolipin, and beta 2 glycoprotein 1 in a Ugandan cohort and their relation to SARS-CoV-2 infection

Research Publication Date:

03/04/2025

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Research Citation:

Epstein-Shuman A, Zhu X, Hunt JH, Fernandez RE, Rozek GM, Redd AD, Gotthold ZA, Quiros G, Galiwango RM, Kigozi G, Caturegli P, Ssekubugu R, Grabowski MK, Chang LW, Reynolds SJ, Laeyendecker O; Rakai Health Science Program. Autoantibodies to interferon alpha, nuclear antigens, cardiolipin, and beta 2 glycoprotein 1 in a Ugandan cohort and their relation to SARS-CoV-2 infection. J Infect Public Health. 2025 Mar 4;18(6):102722. doi: 10.1016/j.jiph.2025.102722. Epub ahead of print. PMID: 40086141.

Research Abstract

Objective: Autoantibodies (AAbs) to interferon alpha, nuclear antigens, cardiolipin, and beta 2 glycoprotein 1, have been associated with COVID-19 severity. Despite relatively low COVID-19 morbidity and mortality in East and Central Africa, AAb prevalence in these populations remain understudied.

Methods: We evaluated AAb seroprevalence in 155 Ugandans, aged 40-50, using paired samples collected before and after the onset of the COVID-19 pandemic. Among these, 117 had serological evidence of SARS-CoV-2 infection, and 38 did not. To assess the effect of SARS-CoV-2 infection on AAb prevalence, we: 1) longitudinally compared AAb prevalence before and after evidence of infection, and 2) cross-sectionally compared AAb prevalence between those with and without infection evidence at both timepoints. Associations between AAbs and health characteristics were also explored.

Results: There was no difference in AAb prevalence between individuals with and without evidence of infection, nor any longitudinal change after evidence of infection. However, we observed a higher-than-expected prevalence anti-beta 2 glycoprotein 1. Additionally, anti-cardiolipin was significantly associated with reported hypertension.

Conclusions: Our findings contribute to the limited literature on AAb prevalence in East Africa and suggest that SARS-CoV-2 does not induce these AAbs.

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https://pubmed.ncbi.nlm.nih.gov/40086141/