Absence of Type I Interferon Autoantibodies or Significant Interferon Signature Alterations in Adults With Post-COVID-19 Syndrome

被引:2
作者
Achleitner, Martin [1 ]
Mair, Nina K. [2 ,3 ,4 ]
Daenhardt, Juliane [1 ]
Kardashi, Romina [1 ]
Puhan, Milo A. [5 ]
Abela, Irene A. [2 ,6 ]
Toepfner, Nicole [7 ]
de With, Katja [8 ]
Kanczkowski, Waldemar [1 ]
Jarzebska, Natalia [1 ]
Rodionov, Roman N. [1 ]
Wolf, Christine [7 ]
Lee-Kirsch, Min Ae [7 ]
Steenblock, Charlotte [1 ,12 ]
Hale, Benjamin G. [2 ]
Bornstein, Stefan R. [1 ,9 ,10 ,11 ]
机构
[1] Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Dept Internal Med 3, Dresden, Germany
[2] Univ Zurich, Inst Med Virol, Zurich, Switzerland
[3] ETH, Life Sci Zurich Grad Sch, CH-8057 Zurich, Switzerland
[4] Univ Zurich, Zurich, Switzerland
[5] Univ Zurich, Epidemiol Biostat & Prevent Inst, Zurich, Switzerland
[6] Univ Hosp Zurich, Dept Infect Dis & Hosp Epidemiol, Zurich, Switzerland
[7] Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Dept Pediat, Dresden, Germany
[8] Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Div Infect Dis, Dresden, Germany
[9] Kings Coll London, Fac Life Sci & Med, Sch Cardiovasc & Metab Med & Sci, London, England
[10] Univ Hosp Zurich, Dept Endocrinol Diabetol & Clin Nutr, Zurich, Switzerland
[11] Univ Zurich, Zurich, Switzerland
[12] Tech Univ Dresden, Dept Internal Med 3, Fetscherstr 74, D-01307 Dresden, Germany
来源
OPEN FORUM INFECTIOUS DISEASES | 2024年 / 11卷 / 01期
关键词
autoantibodies; COVID-19; interferon; post-COVID-19; syndrome;
D O I
10.1093/ofid/ofad641
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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-alpha, IFN-beta, and IFN-omega. 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.
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页数:5
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