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The SARS-CoV-2 trigger highlights host interleukin 1 genetics in Epstein-Barr virus reactivation

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SCHNEIDEROVA Petra MIZERA Jan GHARIBIAN Arootin MANUKYAN Gayane RASKA Milan GAJDOS Petr KOSZTYU Petr GENZOR Samuel KUDELKA Milos SOVA Milan SAVARA Jakub BORIKOVA Alena SHRESTHA Bishu MIKULKOVA Zuzana STEPANEK Ladislav KUFA Jiri JAKUBEC Petr KRIEGOVA Eva

Rok publikování 2025
Druh Článek v odborném periodiku
Časopis / Zdroj Cell Reports
Fakulta / Pracoviště MU

Lékařská fakulta

Citace
www https://www.sciencedirect.com/science/article/pii/S2211124725006308?via%3Dihub
Doi https://doi.org/10.1016/j.celrep.2025.115859
Klíčová slova SARS-CoV-2; interleukin 1; Epstein-Barr virus reactivation
Popis Studies in large cohorts exposed to the same triggers associated with Epstein-Barr virus (EBV) reactivation and the follow-up of post-acute outcomes may uncover the pathomechanisms of autoimmune conditions and EBV-related cancer. We investigated a large cohort of individuals infected with SARS-CoV-2 infection reporting long COVID (LC) symptoms for positive serological markers of recent EBV reactivation (viral capsid antigen [VCA] immunoglobulin [Ig]M, VCA IgA, and early antigen D IgG), host interleukin (IL)1 and IL10 genetics, and immune response. Recent EBV reactivation occurs more frequently in individuals with a genetic risk of EBV reactivation in the IL1RN, IL1A, and IL1B genes associated with an elevated ratio of IL-1 receptor antagonist (IL-1Ra)/IL-1 beta and a higher latent EBV load in blood. High levels of anti-VCA IgA serve as a strong marker of recent EBV reactivation, which is associated with objective long-term pulmonary dysfunction in LC. Our data highlight the association between host IL1 genetics and EBV reactivation.

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