水痘-带状疱疹病毒（varicella-zoster virus，VZV）原发性感染通常会引起儿童期水痘，之后病毒可潜伏于人类外周神经节中，在数十年后重新激活造成带状疱疹，也与危及生命的脑炎、血管病变和脑膜炎等疾病有关。VZV潜伏和再激活的机制尚未得到很好的解释，原因之一是VZV只感染人类，无法使用大多数动物及动物来源的神经元模型。越来越多的证据表明，VZV潜伏是表观遗传学调控的，可用于信号通路分析和表观遗传调节鉴定的体外模型为探索VZV潜伏与再激活机制提供帮助。此文综述了VZV的分子生物学和VZV潜伏与再激活机制方面的研究进展，并提出了未来的研究方向。

Varicella-zoster virus (VZV) primary infection causes varicella (chickenpox) in early period of life. VZV can embed in human peripheral ganglia for decades and then reactivate to cause herpes zoster. It is also associated with life-threatening diseases such as encephalitis, vasculopathy, and meningitis. The mechanisms of VZV latency and reactivation are not well characterized. This is partly due to the human-specific infecting nature of VZV that precludes the use of most animal and animal-derived neuronal models. There is increasing evidence that VZV latency is epigenetically regulated. In vitro models that permit pathway analysis and identification of epigenetic modulations facilitate our understanding of VZV latency. This review summarizes the molecular biology of VZV and its latency and reactivation mechanism, and presents directions for future study.