Permissivity of primary hepatocytes and hepatoma cell lines to support hepatitis C virus infection

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

doi:10.1099/vir.0.000085

Permissivity of primary hepatocytes and hepatoma cell lines to support hepatitis C virus infection

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

^*Corresponding author for this work

King's College London

Research output: Contribution to journal › Article › peer-review

2 Citations (Scopus)

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.

Original language	English
Pages (from-to)	1369-1373
Number of pages	5
Journal	The Journal of general virology
Volume	96
DOIs	https://doi.org/10.1099/vir.0.000085
Publication status	Published - 1 Jun 2015

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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.",

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AU - Wilson, Garrick K.

AU - Farquhar, Michelle J.

AU - Meredith, Luke

AU - Dhawan, Anil

AU - Mitry, Ragai

AU - Balfe, Peter

AU - McKeating, Jane A.

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N2 - 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.

AB - 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.

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Permissivity of primary hepatocytes and hepatoma cell lines to support hepatitis C virus infection

Abstract

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