期刊
VIRUSES-BASEL
卷 13, 期 9, 页码 -出版社
MDPI
DOI: 10.3390/v13091836
关键词
herpes simplex virus; RNA polymerase II; transcription; host shutoff; promoter-proximal pausing; C-terminal domain; polyadenylation; splicing
类别
资金
- Deutsche Forschungsgemeinschaft (DFG) [DO1275/6-1]
- European Union [ERC-2016-CoG 721016-HERPES]
- Alexander von Humboldt Foundation
- German Federal Foreign Office
The review highlights the various impacts of HSV on RNA Polymerase II in infected cells, including changes in Pol II holoenzymes, post-translational modifications, and regulation by viral proteins. The discussion also covers specific activities such as promoter-proximal pausing, splicing, histone repositioning, and termination in relation to host genes. Technological innovations have recently reshaped understanding of previous observations and provide insights for future research directions and considerations.
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.
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