An Evolutionary View of the Arms Race between Protein Kinase R and Large DNA Viruses

被引：5
|
作者：
Carpentier, Kathryn S. [1 ,2 ,3 ]
Geballe, Adam P. [1 ,2 ,3 ]
机构：
[1] Univ Washington, Dept Microbiol & Med, Seattle, WA 98195 USA
[2] Fred Hutchinson Canc Res Ctr, Div Human Biol, 1124 Columbia St, Seattle, WA 98104 USA
[3] Fred Hutchinson Canc Res Ctr, Div Clin Res, 1124 Columbia St, Seattle, WA 98104 USA
来源：
JOURNAL OF VIROLOGY | 2016年 / 90卷 / 07期
基金：
美国国家卫生研究院;
关键词：
DOUBLE-STRANDED-RNA; MURINE CYTOMEGALOVIRUS M142; PKR; TRANSCRIPTION; ANTAGONISM; ACTIVATION; MUTATIONS; DIVERSITY; INFECTION; PATHWAY;
D O I：
10.1128/JVI.01996-15
中图分类号：
Q93 [微生物学];
学科分类号：
071005 ; 100705 ;
摘要：
To establish productive infections, viruses must counteract numerous cellular defenses that are poised to recognize viruses as nonself and to activate antiviral pathways. The opposing goals of host and viral factors lead to evolutionary arms races that can be illuminated by evolutionary and computational methods and tested in experimental models. Here we illustrate how this perspective has been contributing to our understanding of the interactions of the protein kinase R pathway with large DNA viruses.
引用
收藏
页码：3280 / 3283
页数：4
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