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

OVERVIEW 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 vitro systems to study Hepatitis C virus (HCV) replication have demonstrated a role for tetraspanin CD81, scavenger receptor B I (SR-BI) and the tight junction proteins Claudin-1 and Occludin in viral entry, suggesting a multi-step internalization 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.