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脊髓灰质炎病毒蛋白的细胞内分布及病毒特异性细胞质结构的诱导

Intracellular distribution of poliovirus proteins and the induction of virus-specific cytoplasmic structures.

作者信息

Bienz K, Egger D, Rasser Y, Bossart W

出版信息

Virology. 1983 Nov;131(1):39-48. doi: 10.1016/0042-6822(83)90531-7.

Abstract

In a susceptible cell, enteroviruses induce a vesiculated region (the "virus-induced vesicles") which is both the site of viral RNA synthesis as well as the site referred to morphologically, as the "cytopathic effect." Proteins of poliovirus (type I, Mahoney) were shown to migrate into the region of the virus-induced vesicles of infected HEp-2 cells. Five proteins (P2-5b, P3-4b, P3-6a, P3-7c, P3-9) were found to be associated with the vesicles themselves, either as intrinsic membrane protein (P3-9) or in a soluble form within the vesicles (P3-4b, P3-7c, and, partially, P3-6a) or bound to a DOC-resistant structure (P2-5b and a small amount of P3-6a). Partial inhibition of the cleavage of the viral polyprotein with ZnCl2 was used to alter the viral protein pattern within the cells. The data obtained indicate that P2-5b is the protein responsible for the formation of the virus-induced vesicles.

摘要

在易感细胞中,肠道病毒诱导形成一个囊泡化区域(“病毒诱导的囊泡”),该区域既是病毒RNA合成的场所,也是形态学上称为“细胞病变效应”的部位。脊髓灰质炎病毒(I型,马奥尼株)的蛋白质被证明会迁移到感染的HEp-2细胞的病毒诱导囊泡区域。发现有五种蛋白质(P2-5b、P3-4b、P3-6a、P3-7c、P3-9)与囊泡本身相关,要么作为内在膜蛋白(P3-9),要么以可溶形式存在于囊泡内(P3-4b、P3-7c以及部分P3-6a),要么与一种对去氧胆酸钠(DOC)有抗性的结构结合(P2-5b和少量P3-6a)。用氯化锌部分抑制病毒多聚蛋白的切割,以改变细胞内的病毒蛋白模式。所获得的数据表明,P2-5b是负责形成病毒诱导囊泡的蛋白质。

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