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[Us3蛋白激酶调节1型单纯疱疹病毒致病性的分子机制]

[Molecular mechanism by which Us3 protein kinase regulates the pathogenicity of herpes simplex virus type-1].

作者信息

Kato Akihisa

机构信息

Division of Molecular Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo.

出版信息

Uirusu. 2016;66(1):83-90. doi: 10.2222/jsv.66.83.

DOI:10.2222/jsv.66.83
PMID:28484184
Abstract

Herpes simplex virus type-1 (HSV-1) causes a range of human diseases, from mild uncomplicated mucocutaneous infection to life-threatening ones. The Us3 gene of HSV-1 encodes a serine/threonine protein kinase that is highly conserved among alphaherpesviruses. Accumulating evidence suggests that Us3 is a critical regulator of HSV-1 infection; however, the molecular mechanism by which Us3 regulates HSV-1 pathogenicity remains to be elucidated. This article presents a brief summary of the present knowledge on the roles of HSV-1 Us3, with a special focus on its relevancy in vivo.

摘要

1型单纯疱疹病毒(HSV-1)可引发一系列人类疾病,从轻度的无并发症黏膜皮肤感染到危及生命的疾病。HSV-1的Us3基因编码一种丝氨酸/苏氨酸蛋白激酶,该激酶在α疱疹病毒中高度保守。越来越多的证据表明,Us3是HSV-1感染的关键调节因子;然而,Us3调节HSV-1致病性的分子机制仍有待阐明。本文简要总结了目前关于HSV-1 Us3作用的知识,特别关注其在体内的相关性。

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[Molecular mechanism by which Us3 protein kinase regulates the pathogenicity of herpes simplex virus type-1].[Us3蛋白激酶调节1型单纯疱疹病毒致病性的分子机制]
Uirusu. 2016;66(1):83-90. doi: 10.2222/jsv.66.83.
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The UL13 and US3 Protein Kinases of Herpes Simplex Virus 1 Cooperate to Promote the Assembly and Release of Mature, Infectious Virions.单纯疱疹病毒1型的UL13和US3蛋白激酶协同作用以促进成熟感染性病毒粒子的组装和释放。
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Differences in the regulatory and functional effects of the Us3 protein kinase activities of herpes simplex virus 1 and 2.单纯疱疹病毒1型和2型的Us3蛋白激酶活性在调节和功能效应上的差异。
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