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风疹病毒感染过程中细胞内 G3BP 重分布分析。

Analysis of subcellular G3BP redistribution during rubella virus infection.

机构信息

Georgia State University, Department of Biology, Atlanta, GA 30303, USA.

出版信息

J Gen Virol. 2012 Feb;93(Pt 2):267-274. doi: 10.1099/vir.0.036780-0. Epub 2011 Oct 12.

Abstract

Rubella virus (RUBV) replicates slowly and to low titre in vertebrate cultured cells, with minimal cytopathology. To determine whether a cellular stress response is induced during such an infection, the formation of Ras-GAP-SH3 domain-binding protein (G3BP)-containing stress granules (SGs) in RUBV-infected cells was examined. Late in infection, accumulation of G3BP granules was detected, albeit in fewer than half of infected cells. Active virus RNA replication was required for induction of these granules, but they were found to differ from SGs induced by arsenite treatment both in composition (they did not uniformly contain other SG proteins, such as PABP and TIA-1) and in resistance to cycloheximide treatment. Thus, bona fide SGs do not appear to be induced during RUBV infection. The distribution of G3BP, either on its own or in granules, did not overlap with that of dsRNA-containing replication complexes, indicating that it played no role in virus RNA synthesis. However, G3BP did co-localize with viral ssRNAs in perinuclear clusters, suggesting an interaction that could possibly be important in a post-replicative role in virus replication, such as encapsidation.

摘要

风疹病毒(RUBV)在脊椎动物培养细胞中复制缓慢,滴度低,细胞病变最小。为了确定在此种感染过程中是否诱导了细胞应激反应,研究了 RUBV 感染细胞中 Ras-GAP-SH3 结构域结合蛋白(G3BP)包含的应激颗粒(SGs)的形成。在感染后期,尽管只有不到一半的感染细胞中检测到 G3BP 颗粒的积累,但仍检测到了它们的积累。这些颗粒的诱导需要活跃的病毒 RNA 复制,但它们与亚砷酸盐处理诱导的 SG 不同,无论是在组成(它们不均匀地包含其他 SG 蛋白,如 PABP 和 TIA-1)还是在对环已酰亚胺处理的抗性方面。因此,在 RUBV 感染过程中似乎不会诱导真正的 SG。G3BP 的分布(单独或在颗粒中)与包含双链 RNA 的复制复合物不重叠,表明它在病毒 RNA 合成中没有作用。然而,G3BP 确实与核周聚集中的病毒 ssRNA 共定位,表明可能在病毒复制的复制后作用中存在相互作用,例如包裹。

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本文引用的文献

1
Analysis of the function of cytoplasmic fibers formed by the rubella virus nonstructural replicase proteins.
Virology. 2010 Oct 25;406(2):212-27. doi: 10.1016/j.virol.2010.07.025. Epub 2010 Aug 8.
3
Determinants of subcellular localization of the rubella virus nonstructural replicase proteins.
Virology. 2009 Aug 1;390(2):315-23. doi: 10.1016/j.virol.2009.05.019. Epub 2009 Jun 18.
5
Different types of nsP3-containing protein complexes in Sindbis virus-infected cells.
J Virol. 2008 Oct;82(20):10088-101. doi: 10.1128/JVI.01011-08. Epub 2008 Aug 6.
6
P bodies, stress granules, and viral life cycles.
Cell Host Microbe. 2008 Apr 17;3(4):206-12. doi: 10.1016/j.chom.2008.03.004.
7
Rubella virus capsid protein interacts with poly(a)-binding protein and inhibits translation.
J Virol. 2008 May;82(9):4284-94. doi: 10.1128/JVI.02732-07. Epub 2008 Feb 27.
8
Inhibition of cytoplasmic mRNA stress granule formation by a viral proteinase.
Cell Host Microbe. 2007 Nov 15;2(5):295-305. doi: 10.1016/j.chom.2007.08.006.

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