DNA repair proteins affect the lifecycle of herpes simplex virus 1

被引：201

作者：

Lilley, CE

Carson, CT

Muotri, AR

Gage, FH

Weitzman, MD

机构：

[1] Salk Inst Biol Studies, Genet Lab, La Jolla, CA 92037 USA

[2] Univ Calif San Diego, Dept Biol, La Jolla, CA 92093 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2005年 / 102卷 / 16期

基金：

英国惠康基金;

关键词：

replication; Mre11; damage; signaling; ataxia telangiectasia mutated;

D O I：

10.1073/pnas.0501916102

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

We report that herpes simplex virus 1 (HSV-1)infection can activate and exploit a cellular DNA damage response that aids viral replication in nonneuronal cells. Early in HSV-1 infection, several members of the cellular DNA damage-sensing machinery are activated and accumulate at sites of viral DNA replication. When this cellular response is abrogated, formation of HSV-1 replication centers is retarded, and viral production is compromised. In neurons, HSV-1 replication centers fail to mature, and the DNA damage response is not initiated. These data suggest that the failure of neurons to mount a DNA damage response to HSV-1 may contribute to the establishment of latency.

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收藏

页码：5844 / 5849

页数：6

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