Generation of Infectious Hepatitis C Virus in Immortalized Human Hepatocytes

Kanda, Tatsuo; Basu, Arnab; Steele, Robert; Wakita, Takaji; Ryerse, Jan S.; Ray, Ranjit; Ray, Ratna B.

doi:10.1128/jvi.80.9.4633-4639.2006

Cited by 85 publications

(113 citation statements)

References 33 publications

(41 reference statements)

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“…Expression of HCV core protein as well as HCV full-length protein leads to activation of the AR signaling pathway in the presence of androgen [43]. Cell culture-grown HCV infection in human hepatocytes also augments AR-mediated signaling in the presence of androgen [43,44]. These results showed that HCV core protein might cross-talk with the AR signaling pathway for promotion of carcinogenesis.…”

Section: Androgen Receptor-mediating Signaling In Hcvrelated Hepatocamentioning

confidence: 57%

Androgen Receptor and Hepatocellular Carcinoma

Kanda¹

2013

J Gastrointest Dig Syst

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Section: Androgen Receptor-mediating Signaling In Hcvrelated Hepatocamentioning

confidence: 57%

Androgen Receptor and Hepatocellular Carcinoma

Kanda¹

2013

J Gastrointest Dig Syst

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“…2 and 3), a distinct advantage of our assay over other assays using surrogate viruses. A cell culture system for the growth of HCV has also been developed using unique clones derived from HCV strains (15,16). The genetic basis for the propagation of these specific clones and the lack of propagation of most other HCVs in culture are not understood in detail.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, several assay systems, such as recombinant HCV envelope glycoproteins (13,14), HCV pseudotyped particles (4,5), and cell culture-derived infectious HCV particles (15,16), have been developed to study HCV-host cell interactions. These systems have allowed the identification of cell surface molecules, such as CD81 (13), scavenger receptor class B type I (14), claudin-1 (17), occludin (18), dendritic cell/liver-specific ICAM-3 grabbing nonintegrin (19), low density lipoprotein receptor (20), and heparan sulfate (21), that are involved in the mechanism of HCV entry into cells.…”

Section: Hepatitis C Virus (Hcv) Belongs To the Genusmentioning

confidence: 99%

Development of an Infectious Surrogate Hepatitis C Virus Based on a Recombinant Vesicular Stomatitis Virus Expressing Hepatitis C Virus Envelope Glycoproteins and Green Fluorescent Protein

et al. 2015

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SUMMARY:To develop surrogate viruses for hepatitis C virus (HCV), we previously produced recombinant vesicular stomatitis viruses (rVSVs) lacking glycoprotein G but instead expressing chimeric HCV E1/E2 fused to G. These rVSVs were not infectious in HCV-susceptible hepatoma cells. In this study, to develop an infectious surrogate HCV based on an rVSV (vesicular stomatitis virus [VSV]/HCV), we generated a novel rVSV encoding the native E1/E2 (H77 strain) and green fluorescent protein (GFP) instead of G. Here, we showed that this VSV/HCV efficiently infected human hepatoma cells, including Huh7 human hepatoma cells, expressed GFP in these cells, and propagated, but did not do so in nonsusceptible BHK-21 cells. The infectivity of VSV/HCV, measured as the number of foci of GFP-positive cells, was specifically reduced by the addition of chimpanzee anti-HCV serum, anti-E2 antibody, or anti-CD81 antibody to the cultures. When sera obtained from HCV-infected or uninfected patients were added, infection was selectively inhibited only by the sera of HCV-infected patients. These data together suggest that this infectious GFP-expressing VSV/HCV could be a useful tool for studying the mechanisms of HCV entry into cells and for assessing potential inhibitors of viral entry, including neutralizing antibodies.

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“…However, the production of HCV particles in these cells appears to be restricted to a short period not exceeding a few days. Interestingly, recent studies demonstrated that HCV infection triggers in these cells both IFN signaling pathway and an autophagic response (Ait-Goughoulte et al, 2008;Kanda et al, 2006;Kanda et al, 2007). (Carloni et al, 1993;Iacovacci et al, 1997).…”

Section: Human Hepatocarcinoma and Immortalized Hepatocyte (Ihh)-basementioning

confidence: 99%

Cellular models for the screening and development of anti-hepatitis C virus agents

Gondeau

Pichard-Garcia

Maurel

2009

Pharmacology & Therapeutics

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Investigations on the biology of hepatitis C virus (HCV) have been hampered by the lack of small animal models. Efforts have therefore been directed to designing practical and robust cellular models of human origin able to support HCV replication and production in a reproducible, reliable and consistent manner. Many different models based on different forms of virions and hepatoma or other cell types have been described including virus-like particles, pseudotyped particles, subgenomic and full length replicons, virion productive replicons, immortalised hepatocytes, fetal and adult primary human hepatocytes. This review focuses on these different cellular models, their advantages and disadvantages at the biological and experimental levels, and their respective use for evaluating the effect of antiviral molecules on different steps of HCV biology including virus entry, replication, particles generation and excretion, as well as on the modulation by the virus of the host cell response to infection.

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Generation of Infectious Hepatitis C Virus in Immortalized Human Hepatocytes

Abstract: Progress in understanding hepatitis C virus (HCV) biology has remained a challenge due to the lack of an efficient cell culture system for virus growth. In this study, we examined HCV core protein-mediated immortalized human hepatocytes (

Cited by 85 publications

References 33 publications

Androgen Receptor and Hepatocellular Carcinoma

Androgen Receptor and Hepatocellular Carcinoma

Development of an Infectious Surrogate Hepatitis C Virus Based on a Recombinant Vesicular Stomatitis Virus Expressing Hepatitis C Virus Envelope Glycoproteins and Green Fluorescent Protein

Cellular models for the screening and development of anti-hepatitis C virus agents

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