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病毒蛋白酶对细胞质mRNA应激颗粒形成的抑制作用。

Inhibition of cytoplasmic mRNA stress granule formation by a viral proteinase.

作者信息

White James P, Cardenas Ana Maria, Marissen Wilfred E, Lloyd Richard E

机构信息

Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030, USA.

出版信息

Cell Host Microbe. 2007 Nov 15;2(5):295-305. doi: 10.1016/j.chom.2007.08.006.

Abstract

Mammalian cells form dynamic cytoplasmic mRNA stress granules (SGs) in response to environmental stresses including viral infections. SGs are involved in regulating host mRNA function and metabolism, although their precise role during viral infection is unknown. SGs are thought to assemble based on functions of the RNA-binding proteins TIA-1/TIAR or Ras-GAP SH3 domain-binding protein (G3BP). Here, we investigated the relationship between a prototypical plus-strand RNA virus and SGs. Early during poliovirus infection, SG formation is induced, but as infection proceeds this ability is lost, and SGs disperse. Infection resulted in cleavage of G3BP, but not TIA-1 or TIAR, by poliovirus 3C proteinase. Expression of a cleavage-resistant G3BP restored SG formation during poliovirus infection and significantly inhibited virus replication. These results elucidate a mechanism for viral interference with mRNP metabolism and gene regulation and support a critical role of G3BP in SG formation and restriction of virus replication.

摘要

哺乳动物细胞在应对包括病毒感染在内的环境压力时会形成动态的细胞质信使核糖核酸应激颗粒(SGs)。SGs参与调节宿主信使核糖核酸的功能和代谢,尽管它们在病毒感染期间的确切作用尚不清楚。人们认为SGs是基于RNA结合蛋白TIA-1/TIAR或Ras-GAP SH3结构域结合蛋白(G3BP)的功能组装而成。在此,我们研究了一种典型的正链RNA病毒与SGs之间的关系。在脊髓灰质炎病毒感染早期,会诱导SG形成,但随着感染的进行,这种能力会丧失,SGs会分散。感染导致脊髓灰质炎病毒3C蛋白酶切割G3BP,但不切割TIA-1或TIAR。表达抗切割的G3BP可在脊髓灰质炎病毒感染期间恢复SG形成,并显著抑制病毒复制。这些结果阐明了病毒干扰信使核糖核蛋白代谢和基因调控的机制,并支持G3BP在SG形成和限制病毒复制中的关键作用。

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