Varicella Zoster Virus and Stroke: An Intricate Relationship

Varicella Zoster Virus (VZV), responsible for chickenpox and herpes zoster, has emerged as a significant contributor to cerebrovascular disease. Mounting evidence indicates that VZV reactivation may precipitate ischemic and hemorrhagic stroke through mechanisms of viral vasculopathy, immune evasion, and vascular inflammation. While antiviral therapy remains the cornerstone of treatment, several adjunctive regimens exhibit encouraging results in controlling endothelial inflammatory response. This targeted review synthesized findings from 31 studies, including clinical cohorts, in vitro models, and pathological analyses, to evaluate the relationship between VZV and stroke, with emphasis on treatment management beyond antivirals. Evidence demonstrates that VZV antigens are frequently detected within cerebral arteries, where they induce transmural inflammation, endothelial dysfunction, and thrombosis, thereby increasing stroke risk, particularly in the weeks following herpes zoster. Adjunctive therapies such as corticosteroids, statins, and resveratrol show promise in mitigating vascular inflammation, though clinical validation is limited. Preventive measures, especially zoster vaccination, significantly reduce herpes zoster incidence and may lower subsequent stroke risk, yet global uptake remains insufficient. Collectively, the data underscore the need for improved diagnostic tools, combination treatment strategies, and expanded vaccination programs to address the substantial public health burden of VZV-associated stroke.