PDF(Pubmed)
Abstract：
During severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, the viral proteins intimately interact with host factors to remodel the endomembrane system at various steps of the viral lifecycle. The entry of SARS-CoV-2 can be mediated by endocytosis-mediated internalization. Virus-containing endosomes then fuse with lysosomes, in which the viral S protein is cleaved to trigger membrane fusion. Double-membrane vesicles generated from the ER serve as platforms for viral replication and transcription. Virions are assembled at the ER-Golgi intermediate compartment and released through the secretory pathway and/or lysosome-mediated exocytosis. In this review, we will focus on how SARS-CoV-2 viral proteins collaborate with host factors to remodel the endomembrane system for viral entry, replication, assembly and egress. We will also describe how viral proteins hijack the host cell surveillance system-the autophagic degradation pathway-to evade destruction and benefit virus production. Finally, potential antiviral therapies targeting the host cell endomembrane system will be discussed.
摘要：
在严重急性呼吸综合征冠状病毒2（SARS-CoV-2）感染期间，病毒蛋白与宿主因子紧密相互作用，在病毒生命周期的各个步骤重塑内膜系统。SARS-CoV-2的进入可以通过胞吞介导的内化来介导。然后含病毒的内体与溶酶体融合，其中病毒S蛋白被切割以触发膜融合。由ER产生的双膜囊泡充当病毒复制和转录的平台。病毒体在ER-高尔基体中间区室组装并通过分泌途径和/或溶酶体介导的胞吐作用释放。在这次审查中,我们将专注于SARS-CoV-2病毒蛋白如何与宿主因子合作以重塑病毒进入的内膜系统，复制,组装和出口。我们还将描述病毒蛋白如何劫持宿主细胞监测系统-自噬降解途径-以逃避破坏并有益于病毒生产。最后,将讨论针对宿主细胞内膜系统的潜在抗病毒疗法。
