Chromatin dynamics during herpes simplex virus-1 lytic infection

被引:25
作者
Placek, Brandon J.
Berger, Shelley L. [1 ]
机构
[1] Univ Penn, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS | 2010年 / 1799卷 / 3-4期
关键词
HSV-1; Chromatin; Histone variant; Transcription; DNA-DAMAGE RESPONSE; CHECKPOINT SIGNAL-TRANSDUCTION; GENE-EXPRESSION; HISTONE H3; VIRAL REPLICATION; REPAIR PROTEINS; IN-VITRO; TYPE-1; PROMOTERS; GENOME;
D O I
10.1016/j.bbagrm.2010.01.012
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Herpes simplex virus type 1 is a DNA virus that can establish lytic infections in epithelial cells and latent infections in sensory neurons. Upon entry into the nucleus the genome of HSV-1 rapidly associates with histone proteins. Similar to the genomes of the cellular host, HSV-1 is subject to chromatin-based regulation of transcription and replication. However, unlike the host genome, nucleosomes appear to be under-represented on the HSV genome. During lytic infection, when the genome is transcribed, the HSV-1 chromatin structure appears to be disorganized, and characterized by historic variant sub-types and post-translational modifications representative of active chromatin. In contrast, during latency, when the majority of the viral genome is transcriptionally silent, the chromatin is compacted into a regularly repeating. compact heterochromatic structure. Here we discuss recent studies that underscore the importance of chromatin regulation during the lytic phase of the HSV-1 life-cycle. (C) 2010 Published by Elsevier B.V.
引用
收藏
页码:223 / 227
页数:5
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