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      Hepatitis C Virus, Cholesterol and Lipoproteins — Impact for the Viral Life Cycle and Pathogenesis of Liver Disease

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          Abstract

          Hepatitis C virus (HCV) is a leading cause of chronic liver disease, including chronic hepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. Hepatitis C infection associates with lipid and lipoprotein metabolism disorders such as hepatic steatosis, hypobetalipoproteinemia, and hypocholesterolemia. Furthermore, virus production is dependent on hepatic very-low-density lipoprotein (VLDL) assembly, and circulating virions are physically associated with lipoproteins in complexes termed lipoviral particles. Evidence has indicated several functional roles for the formation of these complexes, including co-opting of lipoprotein receptors for attachment and entry, concealing epitopes to facilitate immune escape, and hijacking host factors for HCV maturation and secretion. Here, we review the evidence surrounding pathogenesis of the hepatitis C infection regarding lipoprotein engagement, cholesterol and triglyceride regulation, and the molecular mechanisms underlying these effects.

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          Boceprevir for untreated chronic HCV genotype 1 infection.

          Fred Poordad, Jonathan McCone, Bruce Bacon … (2011)
          Peginterferon-ribavirin therapy is the current standard of care for chronic infection with hepatitis C virus (HCV). The rate of sustained virologic response has been below 50% in cases of HCV genotype 1 infection. Boceprevir, a potent oral HCV-protease inhibitor, has been evaluated as an additional treatment in phase 1 and phase 2 studies. We conducted a double-blind study in which previously untreated adults with HCV genotype 1 infection were randomly assigned to one of three groups. In all three groups, peginterferon alfa-2b and ribavirin were administered for 4 weeks (the lead-in period). Subsequently, group 1 (the control group) received placebo plus peginterferon-ribavirin for 44 weeks; group 2 received boceprevir plus peginterferon-ribavirin for 24 weeks, and those with a detectable HCV RNA level between weeks 8 and 24 received placebo plus peginterferon-ribavirin for an additional 20 weeks; and group 3 received boceprevir plus peginterferon-ribavirin for 44 weeks. Nonblack patients and black patients were enrolled and analyzed separately. A total of 938 nonblack and 159 black patients were treated. In the nonblack cohort, a sustained virologic response was achieved in 125 of the 311 patients (40%) in group 1, in 211 of the 316 patients (67%) in group 2 (P<0.001), and in 213 of the 311 patients (68%) in group 3 (P<0.001). In the black cohort, a sustained virologic response was achieved in 12 of the 52 patients (23%) in group 1, in 22 of the 52 patients (42%) in group 2 (P=0.04), and in 29 of the 55 patients (53%) in group 3 (P=0.004). In group 2, a total of 44% of patients received peginterferon-ribavirin for 28 weeks. Anemia led to dose reductions in 13% of controls and 21% of boceprevir recipients, with discontinuations in 1% and 2%, respectively. The addition of boceprevir to standard therapy with peginterferon-ribavirin, as compared with standard therapy alone, significantly increased the rates of sustained virologic response in previously untreated adults with chronic HCV genotype 1 infection. The rates were similar with 24 weeks and 44 weeks of boceprevir. (Funded by Schering-Plough [now Merck]; SPRINT-2 ClinicalTrials.gov number, NCT00705432.).
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            The lipid droplet is an important organelle for hepatitis C virus production.

            Yusuke Miyanari, Kimie Atsuzawa, Nobuteru Usuda … (2007)
            The lipid droplet (LD) is an organelle that is used for the storage of neutral lipids. It dynamically moves through the cytoplasm, interacting with other organelles, including the endoplasmic reticulum (ER). These interactions are thought to facilitate the transport of lipids and proteins to other organelles. The hepatitis C virus (HCV) is a causative agent of chronic liver diseases. HCV capsid protein (Core) associates with the LD, envelope proteins E1 and E2 reside in the ER lumen, and the viral replicase is assumed to localize on ER-derived membranes. How and where HCV particles are assembled, however, is poorly understood. Here, we show that the LD is involved in the production of infectious virus particles. We demonstrate that Core recruits nonstructural (NS) proteins and replication complexes to LD-associated membranes, and that this recruitment is critical for producing infectious viruses. Furthermore, virus particles were observed in close proximity to LDs, indicating that some steps of virus assembly take place around LDs. This study reveals a novel function of LDs in the assembly of infectious HCV and provides a new perspective on how viruses usurp cellular functions.
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              Robust hepatitis C virus infection in vitro.

              Jin Zhong, Pablo Gastaminza, Guofeng Cheng … (2005)
              The absence of a robust cell culture model of hepatitis C virus (HCV) infection has severely limited analysis of the HCV life cycle and the development of effective antivirals and vaccines. Here we report the establishment of a simple yet robust HCV cell culture infection system based on the HCV JFH-1 molecular clone and Huh-7-derived cell lines that allows the production of virus that can be efficiently propagated in tissue culture. This system provides a powerful tool for the analysis of host-virus interactions that should facilitate the discovery of antiviral drugs and vaccines for this important human pathogen.
              Article 0 comments Cited 353 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Viruses
                Journal ID (iso-abbrev): Viruses
                Journal ID (publisher-id): viruses
                Title: Viruses
                Publisher: MDPI
                ISSN (Electronic): 1999-4915
                Publication date (Electronic): 22 May 2013
                Publication date Collection: May 2013
                Volume: 5
                Issue: 5
                Pages: 1292-1324
                Affiliations
                [1 ]Inserm, U1110, Institute of Virology, Strasbourg 67000, France; E-Mails: felmlee@ 123456unistra.fr (D.J.F.); mohamed-lamine.hafirassou@ 123456etu.unistra.fr (M.L.H.); mathieu.lefevre@ 123456etu.unistra.fr (M.L.)
                [2 ]Université de Strasbourg, Strasbourg 67000, France
                [3 ]Pôle Hépato-digestif, Hôpitaux Universitaires de Strasbourg, Strasbourg 67000, France
                Author notes
                [* ] Authors to whom correspondence should be addressed; E-Mails: thomas.baumert@ 123456unistra.fr (T.F.B.); catherine.schuster@ 123456unistra.fr (C.S.); Tel.: +33-3 6885-3741 (C.S.); Fax: +33-3-6885-5805 (T.F.B. and C.S.).
                Article
                Publisher ID: viruses-05-01292
                DOI: 10.3390/v5051292
                PMC ID: 3712309
                PubMed ID: 23698400
                SO-VID: 6ce783d1-2668-44a9-8531-0d64def4e8da
                Copyright © © 2013 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 18 March 2013
                Date revision received : 10 April 2013
                Date accepted : 27 April 2013
                Categories
                Subject: Review

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: hepatitis c virus,lipoproteins,apolipoproteins,apoe,apob,cholesterol,triglyceride,viral attachment,entry,assembly,secretion,viral immune escape,lipid disorder
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: hepatitis c virus, lipoproteins, apolipoproteins, apoe, apob, cholesterol, triglyceride, viral attachment, entry, assembly, secretion, viral immune escape, lipid disorder

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