Post-COVID varicella-zoster virus reactivation: lowering the immunological threshold for latency breakdown.

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.