Varicella zoster virus (VZV) is a pathogenic human herpes virus which causes varicella as a primary infection, following which it becomes latent in peripheral autonomic, sensory, and cranial nerve ganglionic neurons from where it may reactivate after decades to cause herpes zoster. VZV reactivation may also cause a wide spectrum of neurological syndromes, in particular, acute encephalitis and vasculopathy. While there is potentially a large number of coding viral mutations that might predispose certain individuals to VZV infections, in practice, a variety of host factors are the main determinants of VZV infection, both disseminated and specifically affecting the nervous system. Host factors include increasing age with diminished cell-mediated immunity to VZV, several primary immunodeficiency syndromes, secondary immunodeficiency syndromes, and drug-induced immunosuppression. In some cases, the molecular immunological basis underlying the increased risk of VZV infections has been defined, in particular, the role of POL III mutations, but in other cases, the mechanisms have yet to be determined. The role of immunization in immunosuppressed individuals as well as its possible efficacy in preventing both generalized and CNS-specific infections will require further investigation to clarify in such patients.

水痘带状疱疹病毒（VZV）是一种致病性人类疱疹病毒，会导致水痘为主要感染，随后会潜伏在周围的自主神经，感觉神经和颅神经神经节神经元中，在数十年后可能会重新活化，从而导致带状疱疹。VZV激活也可能引起广泛的神经系统综合症，特别是急性脑炎和血管病变。尽管可能存在大量编码病毒突变，可能使某些人容易感染VZV，但实际上，各种宿主因素是VZV感染的主要决定因素，既可以传播也可以特异性影响神经系统。宿主因素包括年龄增长，细胞介导的对VZV的免疫力降低，几种原发性免疫缺陷综合症，继发性免疫缺陷综合症，和药物诱导的免疫抑制。在某些情况下，已经确定了VZV感染风险增加的分子免疫学基础，特别是POL III突变的作用，但在其他情况下，机制尚待确定。免疫在受免疫抑制的个体中的作用及其在预防全身性感染和中枢神经系统特异性感染中可能的功效将需要进一步研究以阐明此类患者。