Lewy Tyler G, Grabowski Jeffrey M, Bloom Marshall E
NIH/NIAID, Rocky Mountain Laboratories, Laboratory of Virology, Biology of Vector-Borne Viruses Section, Hamilton, MT.
Yale J Biol Med. 2017 Jun 23;90(2):291-300. eCollection 2017 Jun.
Flaviviruses have an intimate relationship with their host cells, utilizing host proteins during replication. Much of viral genome replication and virion assembly occurs on and within the endoplasmic reticulum (ER). As a cellular protein folding hub, the ER provides an ideal environment for flaviviruses to replicate. Flaviviruses can interact with several ER processes, including the unfolded protein response (UPR), a cellular stress mechanism responsible for managing unfolded protein accumulation and ER stress. The UPR can alter the ER environment in several ways, including increasing ER volume and quantity of available chaperones, both of which can favor viral replication. BiP, a chaperone and master regulator of the UPR, has been demonstrated to play a key role in several flavivirus infections. Here we describe what is known in regard to BiP, its implicated role with flavivirus infection, and what remains to be discovered.
黄病毒与其宿主细胞关系密切，在复制过程中利用宿主蛋白。病毒基因组的大部分复制和病毒粒子组装发生在内质网（ER）上及内质网内。作为细胞蛋白质折叠中心，内质网为黄病毒复制提供了理想环境。黄病毒可与多种内质网相关过程相互作用，包括未折叠蛋白反应（UPR），这是一种负责处理未折叠蛋白积累和内质网应激的细胞应激机制。未折叠蛋白反应可通过多种方式改变内质网环境，包括增加内质网体积和可用伴侣蛋白数量，这两者都有利于病毒复制。BiP是一种伴侣蛋白，也是未折叠蛋白反应的主要调节因子，已被证明在多种黄病毒感染中起关键作用。在此，我们描述了关于BiP的已知信息、其在黄病毒感染中的潜在作用以及有待发现的内容。
