[The importance of varicella-zoster virus reactivation in adult central nervous system diseases].

Varicella-zoster virus (VZV) establishes lifelong latency in sensory ganglia following primary infection and can reactivate later in life, causing herpes zoster and a wide spectrum of neurological complications. This review summarizes the pathogenesis and clinical manifestations of VZV during primary infection and reactivation, as well as epidemiological changes following the introduction of routine varicella vaccination in Japan. While primary infection in childhood is generally self-limiting, VZV reactivation is increasingly recognized as a cause of diverse neurological disorders, including postherpetic neuralgia, meningitis, encephalitis, myelitis, and VZV-associated vasculopathy leading to ischemic stroke. Recent large-scale epidemiological studies using advanced causal inference approaches have suggested a significant association between VZV reactivation and the risk of dementia. In addition, accumulating evidence indicates that herpes zoster vaccination may reduce not only the incidence of herpes zoster and its complications but also the risk of subsequent dementia. These findings highlight the potential role of VZV reactivation in neurodegenerative processes and suggest that prevention of VZV reactivation may represent a novel strategy for dementia prevention. Given the aging population and increasing burden of neurological diseases, further interdisciplinary research integrating virology, neurology, and epidemiology is warranted to better understand the role of VZV in neurological disorders and to develop effective preventive strategies.