Authors
Xiaolu Li, Shuchang Cheng, Siqi Wang, Kaili Gao, Yang Bai, Sainan Li, Mingchun Gao, Yongli Guo
Published in
Frontiers in cellular and infection microbiology. Volume 16. Pages 1904565. Epub Aug 05, 2026.
Abstract
Herpes zoster (HZ) is the clinically apparent manifestation of latent varicella-zoster virus (VZV) reactivation. Aging and immunosuppression are established risk contexts. SARS-CoV-2 infection has prompted renewed attention to whether acute or post-acute immune changes can reduce the reserve needed to maintain VZV latency. Large observational studies report a modest increase in HZ after COVID-19, most consistently after severe disease or hospitalization and within early post-infection windows. These associations do not establish direct causation or a population-wide shift of HZ toward younger adults. A threshold-lowering interpretation is more consistent with the available evidence: SARS-CoV-2 infection may narrow latency-control reserve through cellular immune disruption, interferon dysregulation, and inflammation, particularly in hosts already affected by comorbidity or treatment-related immunosuppression. Long COVID provides a setting in which persistent immune dysregulation can be studied, but it is not yet a proven causal framework for VZV disease. Post-COVID HZ may therefore represent a clinically visible manifestation of disrupted host-virus homeostasis in susceptible individuals. Prospective studies that combine clinical phenotyping with VZV-specific cellular immune measurements are needed to test this model.
PMID:
42621909
Bibliographic data and abstract were imported from PubMed on 20 Aug 2026.
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