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Precore G1896A mutation is associated with reduced rates of HBsAg seroclearance in treated HIV hepatitis B virus co‐infected patients from Western Africa
Author(s) -
Boyd A.,
Moh R.,
Maylin S.,
Abdou Chekaraou M.,
Mahjoub N.,
Gabillard D.,
Anglaret X.,
Eholié S. P.,
Delaugerre C.,
Danel C.,
Zoulim F.,
Lacombe K.
Publication year - 2018
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/jvh.12914
Subject(s) - hbsag , medicine , hepatitis b virus , hbeag , lamivudine , virology , viral load , gastroenterology , hepatitis b , genotype , immunology , virus , biology , gene , biochemistry
Summary The 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 )‐naïve HIV ‐ HBV co‐infected patients from Côte 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 ( HB eAg) seroclearance (in HB eAg‐positive patients), and hepatitis B surface antigen ( HB sAg) seroclearance was evaluated using Cox proportional hazards regression. At ARV ‐initiation, median HBV ‐ DNA was 6.04 log 10 copies/ mL ( IQR = 3.70‐7.93) with 97.7% harbouring HBV genotype E. Baseline pcG1896A mutation was identified in 51 (59.3%) patients, who were more commonly HB eAg‐negative ( P < .001) and had basal core promotor A1762T/G1764A mutations ( P < .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% vs no pcG1896A = 66.9%, P = .04), but not after adjusting for baseline HBV ‐ DNA levels and anti‐ HBV agent ( P = .2). No difference in cumulative proportion of HB eAg seroclearance was observed between mutation groups (pcG1896A = 57.1% vs no pcG1896A = 54.3%, P = .7). Significantly higher cumulative proportion of HB sAg seroclearance was observed in patients without this mutation (pcG1896A = 0% vs no pcG1896A = 36.9%, P < .001), even after adjusting for baseline HB sAg quantification and anti‐ HBV agent ( P < .001). In conclusion, lacking the pcG1896A mutation before ARV initiation appeared to increase HB sAg seroclearance rates during treatment. The therapeutic implications of this mutation need further exploration in this setting.