8
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      HBV Bypasses the Innate Immune Response and Does Not Protect HCV From Antiviral Activity of Interferon.

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Hepatitis C virus (HCV) infection is sensitive to interferon (IFN)-based therapy, whereas hepatitis B virus (HBV) infection is not. It is unclear whether HBV escapes detection by the IFN-mediated immune response or actively suppresses it. Moreover, little is known on how HBV and HCV influence each other in coinfected cells. We investigated interactions between HBV and the IFN-mediated immune response using HepaRG cells and primary human hepatocytes (PHHs). We analyzed the effects of HBV on HCV replication, and vice versa, at the single-cell level.

          Related collections

          Author and article information

          Journal
          Gastroenterology
          Gastroenterology
          Elsevier BV
          1528-0012
          0016-5085
          May 2018
          : 154
          : 6
          Affiliations
          [1 ] Department of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany; Division of Virus-Associated Carcinogenesis (F170), German Cancer Research Center (DKFZ), Heidelberg, Germany; HBIGS graduate school, Heidelberg, Germany.
          [2 ] Department of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany.
          [3 ] Department of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany; German Centre for Infection Research (DZIF), partner site Heidelberg, Heidelberg, Germany.
          [4 ] Department of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany; Division of Virus-Associated Carcinogenesis (F170), German Cancer Research Center (DKFZ), Heidelberg, Germany.
          [5 ] Research Group "Dynamics of early viral infection and the innate antiviral response", Division Virus-associated carcinogenesis (F170), German Cancer Research Center (DKFZ), Heidelberg, Germany.
          [6 ] Reproductive Biotechnology, School of Life Sciences Weihenstephan, Technical University of Munich, Munich, Germany.
          [7 ] Department of Gastroenterology, Infection and Intoxication, University Hospital Heidelberg, Heidelberg, Germany.
          [8 ] Department of General-, Visceral- and Transplant Surgery, University Hospital Heidelberg, Heidelberg, Germany.
          [9 ] Department of General-, Visceral- and Transplant Surgery, University Hospital Heidelberg, Heidelberg, Germany; Division of Transplant Surgery, Medical University of Graz, Graz, Austria.
          [10 ] Inserm, U1110, Institut de Recherche sur les Maladies Virales et Hépatiques, Université de Strasbourg, Institut Hospitalo-Universitaire, Pôle Hépato-digestif, Nouvel Hôpital Civil, Strasbourg, France.
          [11 ] Department of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany; Research Group "Dynamics of early viral infection and the innate antiviral response", Division Virus-associated carcinogenesis (F170), German Cancer Research Center (DKFZ), Heidelberg, Germany.
          [12 ] Department of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany; Division of Virus-Associated Carcinogenesis (F170), German Cancer Research Center (DKFZ), Heidelberg, Germany; HBIGS graduate school, Heidelberg, Germany; German Centre for Infection Research (DZIF), partner site Heidelberg, Heidelberg, Germany. Electronic address: Ralf.Bartenschlager@med.uni-heidelberg.de.
          Article
          S0016-5085(18)30112-4
          10.1053/j.gastro.2018.01.044
          29410097
          452ece56-118d-4eeb-8cf9-2fcdc5783dad
          History

          Coinfection,RIG-I,PRR,Interferon-stimulated Gene
          Coinfection, RIG-I, PRR, Interferon-stimulated Gene

          Comments

          Comment on this article