Restarting Lytic Gene Transcription at the Onset of Herpes Simplex Virus Reactivation
Restarting Lytic Gene Transcription at the Onset of Herpes Simplex Virus Reactivation
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DOI：
10.1128/jvi.01419-16
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发表时间：
2017-01-01
影响因子：
5.4
通讯作者：
Wilson, Angus C.
中科院分区：
文献类型：
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作者：
Cliffe, Anna R.;Wilson, Angus C.
单纯疱疹病毒（HSV）在人类周围神经的神经元中建立了潜在的储存库。在这种静止状态下，病毒基因组以环状组蛋白相关附加体的形式持续存在，并且病毒裂解周期基因的转录在很大程度上通过表观遗传过程受到抑制。潜伏病毒会定期重新激活，从而激活裂解基因并发生病毒复制。在这篇文章中，我们回顾了最近的证据，表明控制裂解基因初始转录的机制与从头感染的机制不同，并且将重新激活与神经元应激反应途径直接联系起来。我们还讨论了裂解周期基因表达可以与完整的重新激活程序脱钩的证据，主张对潜伏期进行不太尖锐的双峰定义。
Herpes simplex virus (HSV) establishes a latent reservoir in neurons of human peripheral nerves. In this quiescent state, the viral genome persists as a circular, histone-associated episome, and transcription of viral lytic cycle genes is largely suppressed through epigenetic processes. Periodically, latent virus undergoes reactivation whereby lytic genes are activated and viral replication occurs. In this Gem, we review recent evidence that mechanisms governing the initial transcription of lytic genes are distinct from those of de novo infection and directly link reactivation to neuronal stress response pathways. We also discuss evidence that lytic cycle gene expression can be uncoupled from the full reactivation program, arguing for a less sharply bimodal definition of latency.