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dc.rights.licenseopenen_US
dc.contributor.authorBOYD, A.
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorMOH, Desmorys Raoul
dc.contributor.authorMAYLIN, S.
dc.contributor.authorABDOU CHEKARAOU, M.
dc.contributor.authorMAHJOUB, N.
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorGABILLARD, Delphine
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorANGLARET, Xavier
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorEHOLIE, Serge Paul
dc.contributor.authorDELAUGERRE, C.
dc.contributor.authorDANEL, C.
dc.contributor.authorZOULIM, F.
dc.contributor.authorLACOMBE, K.
dc.date.accessioned2020-10-26T15:04:59Z
dc.date.available2020-10-26T15:04:59Z
dc.date.issued2018-10
dc.identifier.issn1365-2893 (Electronic) 1352-0504 (Linking)en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/11480
dc.description.abstractEnThe nucleotide substitution G1896A on the precore (pc) region has been implicated in virological and serological responses during treatment in hepatitis B virus (HBV)-infected patients. Whether this mutation affects the therapeutic course of HIV-HBV co-infected patients, especially from Western Africa, is unknown. In this prospective cohort study, 86 antiretroviral (ARV)-naive HIV-HBV co-infected patients from Cote d'Ivoire, initiating ARV-treatment containing lamivudine (n=53) or tenofovir (n=33), had available baseline pc sequences. Association of the pcG1896A mutation with time-to-undetectable HBV-DNA, hepatitis B "e" antigen (HBeAg)-seroclearance (in HBeAg-positive patients), and hepatitis B surface antigen (HBsAg)-seroclearance was evaluated using Cox proportional hazards regression. At ARV-initiation, median HBV-DNA was 6.04 log10 copies/mL (IQR=3.70-7.93) with 97.7% harboring HBV genotype E. Baseline pcG1896A mutation was identified in 51 (59.3%) patients, who were more commonly HBeAg-negative (p<0.001) and had basal core promotor A1762T/ G1764A mutations (p<0.001). Patients were followed for a median 36 months (IQR=24-36). Cumulative proportion of undetectable HBV-DNA was significantly higher in patients with baseline mutation (pcG1896A=86.6% versus no pcG1896A=66.9%, p=0.04), but not after adjusting for baseline HBV-DNA levels and anti-HBV agent (p=0.2). No difference in cumulative proportion of HBeAg-seroclearance was observed between mutation groups (pcG1896A=57.1% versus no pcG1896A=54.3%, p=0.7). Significantly higher cumulative proportion of HBsAg-seroclearance was observed in patients without this mutation (pcG1896A=0% versus no pcG1896A=36.9%, p<0.001), even after adjusting for baseline HBsAg-quantification and anti-HBV agent (p<0.001). In conclusion, lacking the pcG1896A mutation before ARV-initiation appeared to increase HBsAg-seroclearance rates during treatment. The therapeutic implications of this mutation need further exploration in this setting.
dc.language.isoENen_US
dc.subject.enIDLIC
dc.title.enPrecore G1896A mutation is associated with reduced rates of HBsAg seroclearance in treated HIV hepatitis B virus co-infected patients from Western Africa
dc.title.alternativeJ Viral Hepaten_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1111/jvh.12914en_US
dc.subject.halSciences du Vivant [q-bio]/Santé publique et épidémiologieen_US
dc.identifier.pubmed29660214en_US
bordeaux.journalJournal of viral hepatitisen_US
bordeaux.page1121-1131en_US
bordeaux.volume25en_US
bordeaux.hal.laboratoriesBordeaux Population Health Research Center (BPH) - U1219en_US
bordeaux.issue10en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.exportfalse
bordeaux.COinSctx_ver=Z39.88-2004&amp;rft_val_fmt=info:ofi/fmt:kev:mtx:journal&amp;rft.jtitle=Journal%20of%20viral%20hepatitis&amp;rft.date=2018-10&amp;rft.volume=25&amp;rft.issue=10&amp;rft.spage=1121-1131&amp;rft.epage=1121-1131&amp;rft.eissn=1365-2893%20(Electronic)%201352-0504%20(Linking)&amp;rft.issn=1365-2893%20(Electronic)%201352-0504%20(Linking)&amp;rft.au=BOYD,%20A.&amp;MOH,%20Desmorys%20Raoul&amp;MAYLIN,%20S.&amp;ABDOU%20CHEKARAOU,%20M.&amp;MAHJOUB,%20N.&amp;rft.genre=article


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