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<publisher>HAL CCSD</publisher>
<title lang=en>Different precore/core mutations of hepatitis B interact with, limit, or favor liver fibrosis severity.</title>
<creator>Ducancelle, Alexandra</creator>
<creator>Pivert, Adeline</creator>
<creator>Bertrais, Sandrine</creator>
<creator>Boursier, Jérôme</creator>
<creator>Balan, Viorica</creator>
<creator>Veillon, Pascal</creator>
<creator>Guillou-Guillemette, Helene, </creator>
<creator>Thibault, Vincent</creator>
<creator>Castelain, Sandrine</creator>
<creator>Roquebert, Bénédicte</creator>
<creator>Coste-Burel, Marianne</creator>
<creator>Mackiewicz, Vincent</creator>
<creator>Schvoerer, Evelyne</creator>
<creator>Larrat, Sylvie</creator>
<creator>Maylin, Sarah</creator>
<creator>Alain, Sophie</creator>
<creator>Loustaud-Ratti, Véronique</creator>
<creator>Gordien, Emmanuel</creator>
<creator>Gozlan, Joël</creator>
<creator>Brodard, Véronique</creator>
<creator>Chevaliez, Stéphane</creator>
<creator>Calès, Paul</creator>
<creator>Lunel-Fabiani, Françoise</creator>
<contributor>Laboratoire HIFIH ; Université d'Angers (UA)</contributor>
<contributor>Centre Hospitalier Universitaire d'Angers (CHU Angers) ; PRES Université Nantes Angers Le Mans [UNAM]</contributor>
<contributor>CHU Pontchaillou [Rennes]</contributor>
<contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Unité de Virologie clinique et fondamentale EA 4294 ; CHU Amiens-Picardie</contributor>
<contributor>Service de microbiologie ; Assistance publique - Hôpitaux de Paris (AP-HP) - Hôpital Bichat - Claude Bernard [Paris]</contributor>
<contributor>Service de virologie [CHU Nantes] ; CHU Nantes</contributor>
<contributor>Hôpital Beaujon</contributor>
<contributor>Laboratoire de Virologie ; CHU Strasbourg</contributor>
<contributor>Unit for Virus Host-Cell Interactions [Grenoble] (UVHCI) ; Université Joseph Fourier - Grenoble 1 (UJF) - European Molecular Biology Laboratory [Grenoble] (EMBL) - Centre National de la Recherche Scientifique (CNRS)</contributor>
<contributor>Laboratoire de Virologie ; Assistance publique - Hôpitaux de Paris (AP-HP) - Groupe Hospitalier Saint-Louis-Lariboisière- Fernand-Widal</contributor>
<contributor>Génétique et Ecologie des Virus, Génétique des Virus et Pathogénèse des Maladies Virales ; Université Paris Diderot - Paris 7 (UPD7) - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>CHU Limoges</contributor>
<contributor>Anti-infectieux : supports moléculaires des résistances et innovations thérapeutiques (RESINFIT) ; Institut National de la Santé et de la Recherche Médicale (INSERM) - Université de Limoges (UNILIM) - Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503)</contributor>
<contributor>Service de bactériologie-Virologie-Hygiène [Avicenne] ; Assistance publique - Hôpitaux de Paris (AP-HP) - Hôpital Avicenne - Université Paris 13 (UP13)</contributor>
<contributor>Laboratoire de virologie ; CHU Saint-Antoine [APHP]</contributor>
<contributor>Centre d'Immunologie et de Maladies Infectieuses (CIMI) ; Université Pierre et Marie Curie - Paris 6 (UPMC) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS)</contributor>
<contributor>Laboratoire de Virologie Médicale et Moléculaire (CardioVir) ; Université de Reims Champagne-Ardenne (URCA) - CHU Reims - SFR CAP Santé (Champagne-Ardenne Picardie Santé) ; Université de Reims Champagne-Ardenne (URCA) - Université de Picardie Jules Verne (UPJV) - Université de Reims Champagne-Ardenne (URCA) - Université de Picardie Jules Verne (UPJV)</contributor>
<contributor>Centre National de Référence Virus des hépatites B, C et Delta ; Institut National de la Transfusion Sanguine [Paris] (INTS) - Assistance publique - Hôpitaux de Paris (AP-HP)</contributor>
<contributor>Institut Mondor de Recherche Biomédicale (IMRB) ; Institut National de la Santé et de la Recherche Médicale (INSERM) - IFR10 - Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)</contributor>
<contributor>Hémodynamique, Interaction Fibrose et Invasivité tumorales Hépatiques (HIFIH) ; PRES Université Nantes Angers Le Mans [UNAM] - IFR 132 - UPRES EA 3859 - Angers Technopole</contributor>
<description>International audience</description>
<source>Journal of gastroenterology and hepatology</source>
<identifier>hal-01477209</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01477209</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01477209</source>
<source>Journal of gastroenterology and hepatology, 2016, 31, pp.1750-1756. 〈10.1111/jgh.13338〉</source>
<identifier>DOI : 10.1111/jgh.13338</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1111/jgh.13338</relation>
<identifier>PUBMED : 26992056</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/26992056</relation>
<language>en</language>
<subject>[SDV.EE] Life Sciences [q-bio]/Ecology, environment</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>BACKGROUND AND AIM: The impact of basal core promoter (BCP) and precore (PC) mutants of the hepatitis B virus (HBV) on liver disease severity remains controversial. The aim of the present study was to screen BCP and PC mutations in 252 HBV surface antigen (HBsAg) positive carriers in France and to assess relationships between these mutations and severe fibrosis. METHODS: Direct sequencing of the precore/core gene was used to detect A1762T/G1764A and G1757A mutations in the BCP and G1896A and G1899A mutations in the PC region. RESULTS: The prevalences of A1762T/G1764A, G1757A, G1896A, and G1899A mutations were 34.1%, 38.7%, 54.9%, and 29.3% (P < 0.001), respectively. The independent predictors of severe fibrosis (>/=F3 Metavir) were older age (P < 0.001), male gender (P = 0.012), elevated alanine aminotransferase (P < 0.001), and the double A1762T/G1764A mutant with no other mutations (P = 0.011). Interestingly, the association of the G1899A mutation with the double A1762T/G1764A mutant significantly counteracted the deleterious effect of the sole double A1762T/G1764A mutant (odds ratio [OR] = 0.28 vs. OR = 3.55, respectively, P = 0.028). CONCLUSIONS: Patients with the A1762T/G1764A mutation have a higher risk of severe fibrosis. The G1899A mutation is a protective factor against severe fibrosis that counteracted the deleterious effect of the A1762T/G1764A mutation. Finally, host phenotypic and HBV genotypic markers independently predict fibrosis severity.</description>
<date>2016</date>
</dc>
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