Stress Granules and Virus Replication.
Stress Granules and Virus Replication.
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DOI：
10.2217/fvl.11.108
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发表时间：
2011
期刊：
影响因子：
3.1
通讯作者：
Miller CL
中科院分区：
文献类型：
--
作者：
Miller CL
病毒依靠细胞翻译机制合成蛋白质。对感染的先天免疫反应的一部分是应激激酶PKR的激活，它使起始因子eIF2的α亚基磷酸化。这导致了翻译的抑制，目的是阻止病毒复制。翻译关闭的下游效应涉及细胞质颗粒的形成，称为应激颗粒（SGs），其中包含mRNA，起始因子，核糖体亚基和其他mRNA调节蛋白。SGs将mrna保持在翻译无活性状态，直到细胞从应激中恢复。最近的研究已经开始阐明SGs对病毒复制的影响。毫不奇怪，已经发现来自不同家族的病毒通过与重要的SG效应蛋白相关联来调节受感染细胞中SG的形成。本文综述了目前关于SGs的知识及其与病毒复制的相互作用和影响。
Viruses are dependent on the cellular translation machinery for protein synthesis. Part of the innate immune response to infection is activation of the stress kinase PKR which phosphorylates the alpha subunit of the initiation factor eIF2. This results in inhibition of translation and is intended to block virus replication. A downstream effect of translational shutoff involves the formation of cytoplasmic granules, termed stress granules (SGs), that contain mRNAs, initiation factors, ribosomal subunits, and other mRNA regulatory proteins. SGs hold mRNAs in a translationally inactive state until cells recover from stress. Recent studies have begun to elucidate the impact of SGs on virus replication. Not surprisingly, viruses from diverse families have been found to modulate SG formation in infected cells by associating with important SG effecter proteins. This review describes the current knowledge on SGs and their interaction with and impact on virus replication.