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      Overview of HCV Life Cycle with a Special Focus on Current and Possible Future Antiviral Targets

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      Author(s): , , , *
      Publication date (Electronic):
      Journal: Viruses
      Publisher: MDPI
      Keywords: HCV, DAA, antiviral targets

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          Abstract

          Hepatitis C infection is the leading cause of liver diseases worldwide and a major health concern that affects an estimated 3% of the global population. Novel therapies available since 2014 and 2017 are very efficient and the WHO considers HCV eradication possible by the year 2030. These treatments are based on the so-called direct acting antivirals (DAAs) that have been developed through research efforts by academia and industry since the 1990s. After a brief overview of the HCV life cycle, we describe here the functions of the different targets of current DAAs, the mode of action of these DAAs and potential future inhibitors.

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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.
          Article 0 comments Cited 369 times – based on 0 reviews     Review now
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            Binding of hepatitis C virus to CD81.

            P Pileri, Y Uematsu, S Campagnoli … (1998)
            Chronic hepatitis C virus (HCV) infection occurs in about 3 percent of the world's population and is a major cause of liver disease. HCV infection is also associated with cryoglobulinemia, a B lymphocyte proliferative disorder. Virus tropism is controversial, and the mechanisms of cell entry remain unknown. The HCV envelope protein E2 binds human CD81, a tetraspanin expressed on various cell types including hepatocytes and B lymphocytes. Binding of E2 was mapped to the major extracellular loop of CD81. Recombinant molecules containing this loop bound HCV and antibodies that neutralize HCV infection in vivo inhibited virus binding to CD81 in vitro.
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              Interferon alfa-2b alone or in combination with ribavirin as initial treatment for chronic hepatitis C. Hepatitis Interventional Therapy Group.

              J. G. McHutchison, S Gordon, E R Schiff … (1998)
              Only 15 to 20 percent of patients with chronic hepatitis C have a sustained virologic response to interferon therapy. We compared the efficacy and safety of recombinant interferon alfa-2b alone with those of a combination of interferon alfa-2b and ribavirin for the initial treatment of patients with chronic hepatitis C. We randomly assigned 912 patients with chronic hepatitis C to receive standard-dose interferon alfa-2b alone or in combination with ribavirin (1000 or 1200 mg orally per day, depending on body weight) for 24 or 48 weeks. Efficacy was assessed by measurements of serum hepatitis C virus (HCV) RNA and serum aminotransferases and by liver biopsy. The rate of sustained virologic response (defined as an undetectable serum HCV RNA level 24 weeks after treatment was completed) was higher among patients who received combination therapy for either 24 weeks (70 of 228 patients, 31 percent) or 48 weeks (87 of 228 patients, 38 percent) than among patients who received interferon alone for either 24 weeks (13 of 231 patients, 6 percent) or 48 weeks (29 of 225 patients, 13 percent) (P<0.001 for the comparison of interferon alone with both 24 weeks and 48 weeks of combination treatment). Among patients with HCV genotype 1 infection, the best response occurred in those who were treated for 48 weeks with interferon and ribavirin. Histologic improvement was more common in patients who were treated with combination therapy for either 24 weeks (57 percent) or 48 weeks (61 percent) than in those who were treated with interferon alone for either 24 weeks (44 percent) or 48 weeks (41 percent). The drug doses had to be reduced and treatment discontinued more often in patients who were treated with combination therapy. In patients with chronic hepatitis C, initial therapy with interferon and ribavirin was more effective than treatment with interferon alone.
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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): 06 January 2019
                Publication date Collection: January 2019
                Volume: 11
                Issue: 1
                Electronic Location Identifier: 30
                Affiliations
                CIRI—Centre International de Recherche en Infectiologie, Univ Lyon, Université Claude Bernard Lyon 1, Inserm, U1111, CNRS, UMR5308, ENS Lyon, F-69007 Lyon, France; nathalie.alazard-dany@ 123456inserm.fr (N.A.-D.); solene.denolly@ 123456ens-lyon.fr (S.D.); bertrand.boson@ 123456ens-lyon.fr (B.B.)
                Author notes
                [* ]Correspondence: flcosset@ 123456ens-lyon.fr
                Author information
                https://orcid.org/0000-0003-1920-5172
                https://orcid.org/0000-0001-8842-3726
                Article
                Publisher ID: viruses-11-00030
                DOI: 10.3390/v11010030
                PMC ID: 6356578
                PubMed ID: 30621318
                SO-VID: 8c566835-48e0-4dd2-84df-766fee45b243
                Copyright © © 2019 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 27 November 2018
                Date accepted : 02 January 2019
                Categories
                Subject: Review

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: hcv,daa,antiviral targets
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: hcv, daa, antiviral targets

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