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痘苗病毒EEV特异性蛋白在细胞内肌动蛋白尾形成和低pH诱导的细胞-细胞融合中的作用。

Roles of vaccinia virus EEV-specific proteins in intracellular actin tail formation and low pH-induced cell-cell fusion.

作者信息

Sanderson C M, Frischknecht F, Way M, Hollinshead M, Smith G L

机构信息

Sir William Dunn School of Pathology, University of Oxford, UK.

出版信息

J Gen Virol. 1998 Jun;79 ( Pt 6):1415-25. doi: 10.1099/0022-1317-79-6-1415.

DOI:10.1099/0022-1317-79-6-1415
PMID:9634084
Abstract

During vaccinia virus (VV) morphogenesis intracellular mature virus (IMV) is wrapped by two additional membranes to form intracellular enveloped virus (IEV). IEV particles can nucleate the formation of actin tails which aid movement of IEVs to the cell surface where the outer IEV membrane fuses with the plasma membrane forming cell-associated enveloped virus (CEV) which remains attached to the cell, or extracellular enveloped virus (EEV) which is shed from the cell. In this report, we have used a collection of VV mutants lacking individual EEV-specific proteins to compare the roles of these proteins in the formation of IEV and IEV-associated actin tails and fusion of infected cells after a low pH shock. Data presented here show that p45-50 (A36R) is not required for IEV formation or for acid-induced cell-cell fusion, but is required for formation of IEV-associated actin tails. In contrast, gp86 (A56R), the virus haemagglutinin, is not required for formation of either IEV or IEV-associated actin tails. Data presented also confirm that p37 (gene F13L), gp42 (B5R) and gp22-24 (A34R) are needed for formation of IEV-associated actin tails and for cell-cell fusion after low pH shock. The phenotypes of these mutants were not affected by the host cell type as similar results were obtained in a range of different cells. Lastly, comparisons of the phenotypes of VV strains Western Reserve, deltaA34R and deltaA36R demonstrate that actin tails are not required for low pH-induced cell-cell fusion.

摘要

在痘苗病毒(VV)形态发生过程中,细胞内成熟病毒(IMV)被另外两层膜包裹形成细胞内包膜病毒(IEV)。IEV颗粒可引发肌动蛋白尾的形成,这有助于IEV向细胞表面移动,在细胞表面,IEV的外膜与质膜融合,形成附着在细胞上的细胞相关包膜病毒(CEV),或从细胞中释放的细胞外包膜病毒(EEV)。在本报告中,我们使用了一系列缺乏单个EEV特异性蛋白的VV突变体,以比较这些蛋白在IEV和IEV相关肌动蛋白尾形成以及低pH冲击后感染细胞融合中的作用。此处呈现的数据表明,p45 - 50(A36R)对于IEV形成或酸诱导的细胞 - 细胞融合不是必需的,但对于IEV相关肌动蛋白尾的形成是必需的。相比之下,病毒血凝素gp86(A56R)对于IEV或IEV相关肌动蛋白尾的形成都不是必需的。所呈现的数据还证实,p37(基因F13L)、gp42(B5R)和gp22 - 24(A34R)对于IEV相关肌动蛋白尾的形成以及低pH冲击后的细胞 - 细胞融合是必需的。这些突变体的表型不受宿主细胞类型的影响,因为在一系列不同细胞中获得了相似的结果。最后,对VV毒株Western Reserve、deltaA34R和deltaA36R表型的比较表明,低pH诱导的细胞 - 细胞融合不需要肌动蛋白尾。

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