Mij
Senior Member (Voting Rights)
Highlights
Host interleukin 1 genetics predisposes individuals to EBV reactivation during COVID-19•
EBV reactivation during SARS-CoV-2 infection contributes to pulmonary long COVID
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High latent EBV loads in blood are associated with long-term lung impairment in long COVID
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Anti-VCA IgA serum levels are a strong marker of recent EBV reactivation
Summary
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-1β 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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