Division of Virology, Department of Pathology, University of Cambridge, Cambridge, UK.
FEMS Microbiol Rev. 2012 May;36(3):684-705. doi: 10.1111/j.1574-6976.2011.00320.x. Epub 2012 Jan 10.
Herpes simplex virus type 1 is a neurotropic herpesvirus that establishes latency within sensory neurones. Following primary infection, the virus replicates productively within mucosal epithelial cells and enters sensory neurones via nerve termini. The virus is then transported to neuronal cell bodies where latency can be established. Periodically, the virus can reactivate to resume its normal lytic cycle gene expression programme and result in the generation of new virus progeny that are transported axonally back to the periphery. The ability to establish lifelong latency within the host and to periodically reactivate to facilitate dissemination is central to the survival strategy of this virus. Although incompletely understood, this review will focus on the mechanisms involved in the regulation of latency that centre on the functions of the virus-encoded latency-associated transcripts (LATs), epigenetic regulation of the latent virus genome and the molecular events that precipitate reactivation.
单纯疱疹病毒 1 型是一种嗜神经疱疹病毒，在感觉神经元内建立潜伏感染。初次感染后，病毒在黏膜上皮细胞内进行有效复制，并通过神经末梢进入感觉神经元。然后，病毒被运送到神经元细胞体，在那里可以建立潜伏感染。病毒周期性地重新激活，恢复其正常的裂解周期基因表达程序，产生新的病毒子代，通过轴突运输回外周。在宿主体内建立终身潜伏感染并周期性重新激活以促进传播的能力是该病毒生存策略的核心。尽管尚未完全了解，但本综述将重点关注调节潜伏感染的机制，这些机制集中在病毒编码的潜伏相关转录物（LATs）的功能、潜伏病毒基因组的表观遗传调控以及引发重新激活的分子事件上。
