Scavenger receptor BI and BII expression levels modulate hepatitis C virus infectivity

摘要: Hepatitis C virus (HCV) enters cells via a pH- and clathrin-dependent endocytic pathway. Scavenger receptor BI (SR-BI) CD81 are important entry factors for HCV internalization into target cells. The SR-BI gene gives rise to at least two mRNA splice variants, SR-BII, which differ in their termini. remains poorly understood, but SR-BII is reported endocytose pathway, making it an attractive internalization. We demonstrate that soluble E2 can interact with human SR-BII. Increased expression of the Huh-7.5 hepatoma cell line enhanced strain J6/JFH JFH infectivity, suggesting endogenous levels these receptors limit infection. Elevated SR-BI, not increased rate infection, may reflect altered intracellular trafficking variants. In plasma, particles have been be complexed lipoproteins, indirect interaction other lipoprotein receptors. Plasma from J6/JFH-infected uPA-SCID mice transplanted hepatocytes demonstrates infectivity SR-BI/II-overexpressing Plasma-derived was inhibited by anti-E2 monoclonal antibody, plasma glycoprotein dependent. Finally, anti-SR-BI antibodies culture- plasma-derived J6/JFH, critical role SR-BI/II