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The Involvement of Tight Junction Protein Claudin-1 in Hepatitis C Virus Entry

机译:紧密连接蛋白Claudin-1参与丙型肝炎病毒的进入

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摘要

Viruses exploit normal cellular processes to accomplish every step in their life Cycle and these processes can differ in diverse cell types. Virus entry into a host cell is defined by specific interaction(s) with cell surface proteins or receptors that confer host and cellular tropism. Recent advances in the development of in krpitro systems to study Hepatitis C virus (HCV) replication have demonstrated role for tetraspanin CD81, scavenger receptor BI (SR-BI) and the tight ction proteins Claudin-1 and Occludin in viral entry, suggesting a multi-step kntemalization process. SR-BI and CD81 bind HCV encoded glycoproteins,suggesting a classical role for these molecules as receptors. In contrast, there is limited evidence for TJ protein association with HCV, which may reflect an indirect role for these proteins in virus internalization.
机译:病毒利用正常的细胞过程来完成生命周期的每个步骤,并且这些过程在不同的细胞类型中可能有所不同。病毒进入宿主细胞的过程是通过与细胞表面蛋白或受体的特异性相互作用来实现的,这些蛋白或受体赋予宿主和细胞嗜性。用于研究丙型肝炎病毒(HCV)复制的krpitro系统开发的最新进展已证明四跨膜CD81,清道夫受体BI(SR-BI)以及紧密连接蛋白Claudin-1和Occludin在病毒进入中的作用,表明存在多种步骤的动词化过程。 SR-BI和CD81结合HCV编码的糖蛋白,暗示这些分子作为受体的经典作用。相反,仅有有限的证据表明TJ蛋白与HCV相关,这可能反映了这些蛋白在病毒内化中的间接作用。

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