Absence of type I interferon autoantibodies or significant interferon signature alterations in adults with post-COVID-19 syndrome
Martin Achleitner, Nina K Mair, Juliane Dänhardt, Romina Kardashi, Milo A Puhan, Irene A Abela, Nicole Toepfner, Katja de With, Waldemar Kanczkowski, Natalia Jarzebska, Roman N Rodionov, Christine Wolf, Min Ae Lee-Kirsch, Charlotte Steenblock, Benjamin G Hale, Stefan R Bornstein- Infectious Diseases
- Oncology
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 impact post-COVID-19 syndrome (PCS), possibly causing persistent fatigue for more than 12 weeks after confirmed SARS-CoV-2 infection. In the current study, we investigated 128 PCS patients, 21 severe COVID-19 survivors, and 38 asymptomatic individuals. We checked for autoantibodies against IFN-α, IFN-β, and IFN-ω. Few PCS patients 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 PCS patients, we evaluated IFN-stimulated gene (ISG) activity and showed that ISG activity didn't correlate with fatigue. In conclusion, impairment of the type I IFN system is unlikely responsible for adult PCS.