During lytic infection, herpes simplex virus (HSV) 1 induces a rapid shutoff of host RNA synthesis while redirecting transcriptional machinery to viral genes. In addition to being a major human pathogen, there is burgeoning clinical interest in HSV as a vector in gene delivery and oncolytic therapies, necessitating research into transcriptional control. This review summarizes the array of impacts that HSV has on RNA Polymerase (Pol) II, which transcribes all mRNA in infected cells. We discuss alterations in Pol II holoenzymes, post-translational modifications, and how viral proteins regulate specific activities such as promoter-proximal pausing, splicing, histone repositioning, and termination with respect to host genes. Recent technological innovations that have reshaped our understanding of previous observations are summarized in detail, along with specific research directions and technical considerations for future studies.

中文翻译：

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单纯疱疹病毒1对宿主转录机制的多管齐下攻击研究进展


在裂解感染期间，单纯疱疹病毒 (HSV) 1 会诱导宿主 RNA 合成快速关闭，同时将转录机制重新定向到病毒基因。除了作为主要的人类病原体之外，临床上对 HSV 作为基因传递和溶瘤治疗载体的兴趣日益浓厚，因此有必要对转录控制进行研究。这篇综述总结了 HSV 对 RNA 聚合酶 (Pol) II 的一系列影响，RNA 聚合酶 II 转录受感染细胞中的所有 mRNA。我们讨论了 Pol II 全酶的改变、翻译后修饰，以及病毒蛋白如何调节特定活性，例如启动子近端暂停、剪接、组蛋白重新定位和宿主基因的终止。详细总结了最近重塑我们对先前观察结果的理解的技术创新，以及未来研究的具体研究方向和技术考虑。