Blázquez Ana-Belén, Escribano-Romero Estela, Merino-Ramos Teresa, Saiz Juan-Carlos, Martín-Acebes Miguel A
Departamento de Biotecnología, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria Madrid, Spain.
Departamento de Biotecnología, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria Madrid, Spain ; Departamento de Virología y Microbiología, Centro de Biología Molecular "Severo Ochoa", Consejo Superior de Investigaciones Científicas - Universidad Autónoma de Madrid Madrid, Spain.
Front Microbiol. 2014 Jun 3;5:266. doi: 10.3389/fmicb.2014.00266. eCollection 2014.
The Flavivirus is a genus of RNA viruses that includes multiple long known human, animal, and zoonotic pathogens such as Dengue virus, yellow fever virus, West Nile virus, or Japanese encephalitis virus, as well as other less known viruses that represent potential threats for human and animal health such as Usutu or Zika viruses. Flavivirus replication is based on endoplasmic reticulum-derived structures. Membrane remodeling and accumulation of viral factors induce endoplasmic reticulum stress that results in activation of a cellular signaling response termed unfolded protein response (UPR), which can be modulated by the viruses for their own benefit. Concomitant with the activation of the UPR, an upregulation of the autophagic pathway in cells infected with different flaviviruses has also been described. This review addresses the current knowledge of the relationship between endoplasmic reticulum stress, UPR, and autophagy in flavivirus-infected cells and the growing evidences for an involvement of these cellular pathways in the replication and pathogenesis of these viruses.
黄病毒属是一类RNA病毒,包括多种早已为人所知的人类、动物和人畜共患病原体,如登革病毒、黄热病毒、西尼罗河病毒或日本脑炎病毒,以及其他不太知名但对人类和动物健康构成潜在威胁的病毒,如乌苏图病毒或寨卡病毒。黄病毒的复制基于内质网衍生结构。膜重塑和病毒因子的积累会诱导内质网应激,从而导致一种称为未折叠蛋白反应(UPR)的细胞信号反应被激活,病毒可对其进行调节以自身受益。与UPR的激活同时,在感染不同黄病毒的细胞中,自噬途径的上调也有报道。本综述阐述了目前关于内质网应激、UPR和自噬在黄病毒感染细胞中的关系的知识,以及越来越多的证据表明这些细胞途径参与了这些病毒的复制和发病机制。