Hammerschmidt Wolfgang
Research Unit Gene Vectors, Helmholtz Zentrum München, German Research Center for Environmental Health, and German Centre for Infection Research (DZIF), Partner site Munich, Marchioninistr. 25, 81377, Munich, Germany.
Curr Top Microbiol Immunol. 2015;390(Pt 1):103-17. doi: 10.1007/978-3-319-22822-8_6.
Ever since the discovery of Epstein-Barr virus (EBV) more than 50 years ago, this virus has been studied for its capacity to readily establish a latent infection, which is the prominent hallmark of this member of the herpesvirus family. EBV has become an important model for many aspects of herpesviral latency, but the molecular steps and mechanisms that lead to and promote viral latency have only emerged recently. It now appears that the virus exploits diverse facets of epigenetic gene regulation in the cellular host to establish a latent infection. Most viral genes are transcriptionally repressed, and viral chromatin is densely compacted during EBV's latent phase, but latent infection is not a dead end. In order to escape from this phase, epigenetic silencing must be reverted efficiently and quickly. It appears that EBV has perfected a clever strategy to overcome transcriptional repression of its many lytic genes to initiate virus de novo synthesis within a few hours after induction of its lytic cycle. This review tries to summarize the known molecular mechanisms, the current models, concepts, and ideas underlying this viral strategy. This review also attempts to identify and address gaps in our current understanding of EBV's epigenetic mechanisms within the infected cellular host.
自50多年前发现爱泼斯坦-巴尔病毒（EBV）以来，人们一直在研究这种病毒易于建立潜伏感染的能力，这是疱疹病毒家族这一成员的显著特征。EBV已成为疱疹病毒潜伏多个方面的重要模型，但导致并促进病毒潜伏的分子步骤和机制直到最近才逐渐明晰。现在看来，该病毒利用细胞宿主中表观遗传基因调控的多个方面来建立潜伏感染。在EBV的潜伏阶段，大多数病毒基因的转录受到抑制，病毒染色质紧密压缩，但潜伏感染并非绝境。为了从这个阶段逃脱，表观遗传沉默必须高效且迅速地逆转。似乎EBV已经完善了一种巧妙的策略，以克服其许多裂解基因的转录抑制，从而在诱导其裂解周期后的几小时内启动病毒的从头合成。本综述试图总结已知的分子机制、当前的模型、概念以及这种病毒策略背后的观点。本综述还试图识别并解决我们目前对受感染细胞宿主内EBV表观遗传机制理解上的空白。
