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Virology. 2016 Feb;489:75-85. doi: 10.1016/j.virol.2015.11.032. Epub 2015 Dec 21.
2
Knockout of the Host Resistance Gene Pkr Fully Restores Replication of Murine Cytomegalovirus m142 and m143 Mutants In Vivo.宿主抗性基因Pkr的敲除可完全恢复小鼠巨细胞病毒m142和m143突变体在体内的复制。
J Virol. 2015 Oct 28;90(2):1144-7. doi: 10.1128/JVI.02003-15. Print 2016 Jan 15.
3
Experimental Evolution Identifies Vaccinia Virus Mutations in A24R and A35R That Antagonize the Protein Kinase R Pathway and Accompany Collapse of an Extragenic Gene Amplification.实验进化鉴定出痘苗病毒A24R和A35R基因中的突变,这些突变拮抗蛋白激酶R通路并伴随一个基因外基因扩增的崩溃。
J Virol. 2015 Oct;89(19):9986-97. doi: 10.1128/JVI.01233-15. Epub 2015 Jul 22.
4
Vaccination with a Live Attenuated Cytomegalovirus Devoid of a Protein Kinase R Inhibitory Gene Results in Reduced Maternal Viremia and Improved Pregnancy Outcome in a Guinea Pig Congenital Infection Model.在豚鼠先天性感染模型中,接种缺乏蛋白激酶R抑制基因的减毒活巨细胞病毒可降低母体病毒血症并改善妊娠结局。
J Virol. 2015 Oct;89(19):9727-38. doi: 10.1128/JVI.01419-15. Epub 2015 Jul 15.
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Double-Stranded RNA Is Detected by Immunofluorescence Analysis in RNA and DNA Virus Infections, Including Those by Negative-Stranded RNA Viruses.在RNA和DNA病毒感染中,包括负链RNA病毒感染,通过免疫荧光分析可检测到双链RNA。
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High-throughput analysis of human cytomegalovirus genome diversity highlights the widespread occurrence of gene-disrupting mutations and pervasive recombination.人类巨细胞病毒基因组多样性的高通量分析突出了基因破坏突变的广泛发生和普遍存在的重组现象。
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蛋白激酶R与大型DNA病毒之间军备竞赛的进化观点

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

作者信息

Carpentier Kathryn S, Geballe Adam P

机构信息

Departments of Microbiology and Medicine, University of Washington, Seattle, Washington, USA Divisions of Human Biology and Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.

Departments of Microbiology and Medicine, University of Washington, Seattle, Washington, USA Divisions of Human Biology and Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA

出版信息

J Virol. 2016 Jan 20;90(7):3280-3. doi: 10.1128/JVI.01996-15.

DOI:10.1128/JVI.01996-15
PMID:26792736
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4794663/
Abstract

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.

摘要

为了建立有效的感染,病毒必须对抗众多细胞防御机制,这些防御机制随时准备将病毒识别为非自身物质并激活抗病毒途径。宿主和病毒因子的相反目标导致了进化军备竞赛,这可以通过进化和计算方法来阐明,并在实验模型中进行测试。在这里,我们阐述了这种观点如何有助于我们理解蛋白激酶R途径与大型DNA病毒的相互作用。