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学科主题基础医学
Disruption of the p53-p21 pathway inhibits efficiency of the lytic-replication cycle of herpes simplex virus type 2 (HSV-2)
Zhou, Qi1; Zhu, Meng1; Zhang, Hao1; Yi, Ting2; Klena, John D.1; Peng, Yihong1
关键词HSV-2 Viral replication p53 p21 siRNAs
刊名VIRUS RESEARCH
2012-10-01
DOI10.1016/j.virusres.2012.07.011
169期:1页:91-97
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Virology
资助者National High-Tech Research and Development Program of China (863 Program) ; National Natural Science Foundation of China ; National High-Tech Research and Development Program of China (863 Program) ; National Natural Science Foundation of China
研究领域[WOS]Virology
关键词[WOS]CELL-CYCLE ; HUMAN CYTOMEGALOVIRUS ; GENE-EXPRESSION ; P53 ACTIVITY ; APOPTOSIS ; P21 ; INFECTION ; PROTEIN ; G(1) ; DNA
英文摘要

Cellular p53 and its downstream mediator p21, the major cellular growth suppression and DNA repair markers, have recently been implicated in viral amplification. Here, we show that herpes simplex virus type 2 (HSV-2) infection of both HCT116 p53(+/+) and NIH3T3 cells resulted in sustained increases of p21. HSV-2 infection did not increase cellular p53 expression, but led to phosphorylation of this protein at Ser20. This phosphorylation was accompanied by the increase of p21 protein levels. Furthermore, specific knockdown of endogenous p21 by siRNAs severely impaired virus production represented by HSV envelope glycoprotein B (gB) expression and progeny virus titers. Disruption of the p53-p21 pathway by either knocking down p53 in HCT116 p53(+/+) and NIH3T3 cells or using p53-deficient HCT116 p53(-/-) cells, led to a significant reduction of HSV-2 production. Together, these results suggest that the p53-p21 pathway is required for efficient HSV-2 lytic replication cycle. Because HSV infection induces the G0/G1 phase arrest at the early step of lytic-replication cycle, we propose that HSV-2 might hijack the cellular p53-p21 pathway to arrest the host cell cycle at G0/G1 phase, blocking cellular DNA synthesis, for its own benefit, i.e., to favor its own viral replication by avoiding competition in generating viral nucleotide pools. (C) 2012 Elsevier B.V. All rights reserved.

语种英语
所属项目编号2007AA02Z317 ; 30470084
资助者National High-Tech Research and Development Program of China (863 Program) ; National Natural Science Foundation of China ; National High-Tech Research and Development Program of China (863 Program) ; National Natural Science Foundation of China
WOS记录号WOS:000311133800012
Citation statistics
Cited Times:1[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/54512
Collection北京大学基础医学院_病原生物学系
作者单位1.Peoples Hosp Yichun City, Yichun 336000, Peoples R China
2.Peking Univ, Sch Basic Med Sci, Dept Microbiol, Beijing 100191, Peoples R China
Recommended Citation
GB/T 7714
Zhou, Qi,Zhu, Meng,Zhang, Hao,et al. Disruption of the p53-p21 pathway inhibits efficiency of the lytic-replication cycle of herpes simplex virus type 2 (HSV-2)[J]. VIRUS RESEARCH,2012,169(1):91-97.
APA Zhou, Qi,Zhu, Meng,Zhang, Hao,Yi, Ting,Klena, John D.,&Peng, Yihong.(2012).Disruption of the p53-p21 pathway inhibits efficiency of the lytic-replication cycle of herpes simplex virus type 2 (HSV-2).VIRUS RESEARCH,169(1),91-97.
MLA Zhou, Qi,et al."Disruption of the p53-p21 pathway inhibits efficiency of the lytic-replication cycle of herpes simplex virus type 2 (HSV-2)".VIRUS RESEARCH 169.1(2012):91-97.
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