Absence of Type I Interferon Autoantibodies or Significant Interferon Signature Alterations in Adults With Post-COVID-19 Syndrome
- PMID: 38179103
- PMCID: PMC10766412
- DOI: 10.1093/ofid/ofad641
Absence of Type I Interferon Autoantibodies or Significant Interferon Signature Alterations in Adults With Post-COVID-19 Syndrome
Abstract
Genetic defects in the interferon (IFN) system or neutralizing autoantibodies against type I IFNs contribute to severe COVID-19. Such autoantibodies were proposed to affect post-COVID-19 syndrome (PCS), possibly causing persistent fatigue for >12 weeks after confirmed SARS-CoV-2 infection. In the current study, we investigated 128 patients with PCS, 21 survivors of severe COVID-19, and 38 individuals who were asymptomatic. We checked for autoantibodies against IFN-α, IFN-β, and IFN-ω. Few patients with PCS had autoantibodies against IFNs but with no neutralizing activity, indicating a limited role of type I IFNs in PCS pathogenesis. In a subset consisting of 28 patients with PCS, we evaluated IFN-stimulated gene activity and showed that it did not correlate with fatigue. In conclusion, impairment of the type I IFN system is unlikely responsible for adult PCS.
Keywords: COVID-19; autoantibodies; interferon; post–COVID-19 syndrome.
© The Author(s) 2023. Published by Oxford University Press on behalf of Infectious Diseases Society of America.
Conflict of interest statement
Potential conflicts of interest. All authors: No reported conflicts.
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- Paludan SR, Mogensen TH. Innate immunological pathways in COVID-19 pathogenesis. Sci Immunol 2022; 7:eabm5505. - PubMed
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