The HCV Life Cycle 丙肝病毒的病毒周期.docx

The HCV Life CycleKey steps in the life cycle of HCV include entry into the host cell, uncoating of the viral genome, translation of viral proteins, viral genome replication, and the assembly and release of virions. All these events occur outside the nucleus of the host cell.Viral EntryVarious factors attributed to the host cell seem necessary to enable HCV entry. The first factor that was identified as necessary for HCV entry was the tetraspanin, CD81. Although CD81 is expressed on many cell types and cannot explain HCVs liver tropism, HCV entry is strongly reduced in the presence of antibodies to CD81, or when CD81 expression is downregulated in hepatoma cells.javascript:newshowcontent(active,references);[3] The human scavenger receptor class B type I (SR-BI) is thought to be an additional factor that might mediate entry of HCV into cells.javascript:newshowcontent(active,references);[4] SR-BI is a physiological HDL(High-density lipoprotein (HDL) is one of the five major groups of /wiki/Lipoproteinlipoproteins, which, in order of sizes, largest to smallest, are /wiki/Chylomicronchylomicrons, /wiki/Very_low-density_lipoproteinVLDL, /wiki/Intermediate-density_lipoproteinIDL, /wiki/Low-density_lipoproteinLDL, and HDL) receptor that mediates selective HDL-cholesterol uptake,javascript:newshowcontent(active,references);[5] but can also bind to other ligands,javascript:newshowcontent(active,references);[6] some of which affect HCV infectivity.javascript:newshowcontent(active,references);[7,8] Plasma-purified HDL enhances the entry of HCV pseudoparticles (HCVpp). This enhancement of HCVpp entry into host cells probably depends on HDL binding to SR-BI, because silencing of SR-BI expression by RNA interference (RNAi) markedly reduces HDL-mediated enhancement of HCVpp entry.javascript:newshowcontent(active,references);[9,10] In 2008, Murao et al. showed that the endogenous expression of SR-BI by hepatocytes is suppressed by exposure to IFN-α,javascript:newshowcontent(active,