REGULATORY T-CELL ACTIVITY AS A MARKER OF POST–COVID-19 AND HERPETIC SECONDARY VASCULITIS IN YOUNG AND MATURE PATIENTS

Background. Post-viral vasculitis represents a heterogeneous inflammatory condition in which persistent immune dysregulation following acute infection or viral reactivation contributes to vascular pathology. SARS-CoV-2, Epstein–Barr virus (EBV), human herpesvirus 6 (HHV-6), and human herpesvirus 7 (HHV-7) are capable of inducing prolonged immune alterations, particularly in mature individuals. Objective. To characterize immune dysregulation in patients with post-viral vasculitis associated with SARS-CoV-2 and herpesvirus reactivation, with emphasis on regulatory T cells, adaptive immune remodeling, innate immune activation, and age-related differences. Methods. Fifty-eight patients with post-viral vasculitis (post–COVID-19, n = 26; EBV/HHV-6/HHV-7, n = 32) and 20 healthy controls underwent extended immunophenotyping by multiparametric flow cytometry. Patients were additionally stratified by age (19–45 and 45–63 years). Results. Post–COVID-19 vasculitis was characterized by reduced regulatory T-cell frequencies and expansion of memoryCD4+ T cells compared with herpesvirus-associated vasculitis. Herpesvirus-associated cases demonstrated pronounced memory T-cell predominance, reduced memory B-cell compartments, and increased cytotoxic NK-cell subsets. Age stratified analysis revealed more severe immune dysregulation in patients aged 45–63 years, with the most pronounced regulatory T-cell depletion observed in post–COVID-19 vasculitis. Conclusions. Post-viral vasculitis exhibits virus-specific and age-dependent immune signatures. SARS-CoV-2–associated vasculitis is marked by profound impairment of immunoregulatory mechanisms, particularly in mature patients, whereas herpesvirus-associated vasculitides demonstrate distinct patterns of adaptive and innate immune activation.