Abstract

The major cell type supporting hepatitis C virus (HCV) infection is the hepatocyte; however, most reports studying viral entry and replication utilize transformed hepatoma cell lines. We demonstrate that HCV pseudoparticles (HCVpp) infect primary hepatocytes with comparable rates to hepatoma cells, demonstrating the limited variability in donor hepatocytes to support HCV receptor-glycoprotein-dependent entry. In contrast, we observed a 2-log range in viral replication between the same donor hepatocytes. We noted that cell proliferation augments pseudoparticle reporter activity and arresting hepatoma cells yields comparable levels of infection to hepatocytes. This study demonstrates comparable rates of HCVpp entry into primary hepatocytes and hepatoma cells, validating the use of transformed cells as a model system to study HCV entry.

Highlights

  • We demonstrate that hepatitis C virus (HCV) pseudoparticles (HCVpp) infect primary hepatocytes with comparable rates to hepatoma cells, demonstrating the limited variability in donor hepatocytes to support HCV receptor-glycoprotein-dependent entry

  • This study demonstrates comparable rates of HCVpp entry into primary hepatocytes and hepatoma cells, validating the use of transformed cells as a model system to study HCV entry

  • HCV initiates infection by attaching to molecules or receptors at the cell surface and current evidence supports an essential role for scavenger receptor class B member I (SR-BI), tetraspanin CD81 and tight-junction proteins claudin-1 and occludin in clathrindependent particle endocytosis (Meredith et al, 2012; Ploss & Evans, 2012)

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Summary

University of Birmingham

Garrick K; Farquhar, Michelle J; Meredith, Luke; Dhawan, Anil; Mitry, Ragai; Balfe, Peter; McKeating, Jane A.

Short Communication
Findings
Mitomycin C Irradiated
Full Text
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