APA
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Achleitner, M., Mair, N. K., Dänhardt, J., Kardashi, R., Puhan, M., Abela, I., … Bornstein, S. (2023). Absence of Type I Interferon Autoantibodies or Significant Interferon Signature Alterations in Adults With Post–COVID-19 Syndrome. Open Forum Infectious Diseases.
Chicago/Turabian
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Achleitner, Martin, Nina K. Mair, Juliane Dänhardt, Romina Kardashi, M. Puhan, I. Abela, N. Toepfner, et al. “Absence of Type I Interferon Autoantibodies or Significant Interferon Signature Alterations in Adults With Post–COVID-19 Syndrome.” Open Forum Infectious Diseases (2023).
MLA
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Achleitner, Martin, et al. “Absence of Type I Interferon Autoantibodies or Significant Interferon Signature Alterations in Adults With Post–COVID-19 Syndrome.” Open Forum Infectious Diseases, 2023.
BibTeX Click to copy
@article{martin2023a,
title = {Absence of Type I Interferon Autoantibodies or Significant Interferon Signature Alterations in Adults With Post–COVID-19 Syndrome},
year = {2023},
journal = {Open Forum Infectious Diseases},
author = {Achleitner, Martin and Mair, Nina K. and Dänhardt, Juliane and Kardashi, Romina and Puhan, M. and Abela, I. and Toepfner, N. and de With, Katja and Kanczkowski, Waldemar and Jarzebska, N. and Rodionov, R. and Wolf, Christine and Lee-Kirsch, M. and Steenblock, C. and Hale, B. G. and Bornstein, S.}
}
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.