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本文引用的文献

1
Functional genetic and biophysical analyses of membrane disruption by human adenovirus.人类腺病毒通过膜破坏的功能遗传和生物物理分析。
J Virol. 2011 Mar;85(6):2631-41. doi: 10.1128/JVI.02321-10. Epub 2011 Jan 5.
2
A proapoptotic peptide derived from reovirus outer capsid protein {micro}1 has membrane-destabilizing activity.源自呼肠孤病毒外壳蛋白 {micro}1 的促凋亡肽具有破坏膜的活性。
J Virol. 2011 Feb;85(4):1507-16. doi: 10.1128/JVI.01876-10. Epub 2010 Nov 24.
3
N-terminal α-helix-independent membrane interactions facilitate adenovirus protein VI induction of membrane tubule formation.N-端α-螺旋非依赖性膜相互作用促进腺病毒蛋白 VI 诱导膜管形成。
Virology. 2010 Dec 5;408(1):31-8. doi: 10.1016/j.virol.2010.08.033. Epub 2010 Sep 25.
4
An N-terminal domain of adenovirus protein VI fragments membranes by inducing positive membrane curvature.腺病毒蛋白 VI 的 N 端结构域通过诱导正膜曲率来破坏膜。
Virology. 2010 Jun 20;402(1):11-9. doi: 10.1016/j.virol.2010.03.043. Epub 2010 Apr 20.
5
Flock house virus: a model system for understanding non-enveloped virus entry and membrane penetration.禽痘病毒:一种用于理解无包膜病毒进入和膜穿透的模式系统。
Curr Top Microbiol Immunol. 2010;343:1-22. doi: 10.1007/82_2010_35.
6
From touchdown to transcription: the reovirus cell entry pathway.从着陆到转录:呼肠孤病毒的细胞进入途径。
Curr Top Microbiol Immunol. 2010;343:91-119. doi: 10.1007/82_2010_32.
7
Structures and functions of parvovirus capsids and the process of cell infection.细小病毒衣壳的结构与功能及细胞感染过程。
Curr Top Microbiol Immunol. 2010;343:149-76. doi: 10.1007/82_2010_33.
8
Picornaviruses.小核糖核酸病毒。
Curr Top Microbiol Immunol. 2010;343:43-89. doi: 10.1007/82_2010_37.
9
Adenovirus.腺病毒。
Curr Top Microbiol Immunol. 2010;343:195-224. doi: 10.1007/82_2010_16.
10
Cryo-electron microscopy structure of an adenovirus-integrin complex indicates conformational changes in both penton base and integrin.腺病毒-整合素复合物的冷冻电子显微镜结构表明五聚体基底和整合素均发生构象变化。
J Virol. 2009 Nov;83(22):11491-501. doi: 10.1128/JVI.01214-09. Epub 2009 Sep 2.

病毒破坏膜的武器:无包膜病毒穿透膜的可变模式。

Viral weapons of membrane destruction: variable modes of membrane penetration by non-enveloped viruses.

机构信息

Department of Immunology and Microbial Sciences, The Scripps Research Institute, La Jolla, CA 92037, USA.

出版信息

Curr Opin Virol. 2011 Jul;1(1):44-9. doi: 10.1016/j.coviro.2011.05.002.

DOI:10.1016/j.coviro.2011.05.002
PMID:21804909
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3144554/
Abstract

Significant progress has recently been obtained in our understanding of cellular entry by nonenveloped viruses (NEVs). A key step in the entry process involves the disruption or remodeling of the limiting cell membrane allowing the virus to gain access to the cellular replication machinery. Biochemical, genetic and structural data from diverse virus groups have shed light on the process of membrane penetration thereby revealing both the conservation and divergence of the mechanisms and principles governing this process. In general, membrane breach is achieved via the highly regulated spatiotemporal exposure of a virally encoded membrane lytic factor, resulting in the transfer of the viral genome or nucleocapsid into the cytosol.

摘要

近年来,人们对无包膜病毒(NEVs)的细胞进入机制有了更深入的了解。进入过程的一个关键步骤涉及到破坏或重塑限制细胞膜,使病毒能够进入细胞复制机制。来自不同病毒群的生化、遗传和结构数据揭示了膜穿透过程,从而揭示了控制这一过程的机制和原理的保守性和多样性。一般来说,膜破裂是通过病毒编码的膜裂解因子的高度调控时空暴露来实现的,导致病毒基因组或核衣壳转移到细胞质中。