Instituto de Salud Pública, Universidad Veracruzana, Av. Luis Castelazo Ayala s/n, Col. Industrial Ánimas, 91190, Xalapa, Veracruz, México.
Instituto de Biotecnología, Universidad Nacional Autónoma de México, Av. Universidad 2001, 62210, Cuernavaca, Morelos, México.
Viruses. 2011 Nov;3(11):2328-2338. doi: 10.3390/v3112328. Epub 2011 Nov 18.
As intracellular parasites, viruses require a host cell in order to replicate. However, they face a series of cellular responses against infection. One of these responses is the activation of the double-stranded RNA (dsRNA)-activated protein kinase R (PKR). PKR phosphorylates the α subunit of eukaryotic translation initiation factor 2 (eIF2α), which in turn results in global protein synthesis inhibition and formation of stress granules (SGs). Recent studies have shown that SGs can interfere with the replicative cycle of certain viruses. This review addresses how viruses have evolved different control strategies at the SG level to ensure an efficient replication cycle during the cellular stress response triggered by the viral infection.
作为细胞内寄生虫,病毒需要宿主细胞才能进行复制。然而,它们面临着一系列针对感染的细胞反应。其中一种反应是双链 RNA (dsRNA)-激活的蛋白激酶 R (PKR)的激活。PKR 磷酸化真核翻译起始因子 2 (eIF2α)的α亚基,进而导致全局蛋白质合成抑制和应激颗粒 (SGs)的形成。最近的研究表明,SGs 可以干扰某些病毒的复制周期。这篇综述探讨了病毒如何在 SG 水平上进化出不同的控制策略,以确保在病毒感染引发的细胞应激反应中,复制周期的有效进行。