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Hepatitis B virus genotype G and liver fibrosis progression in chronic hepatitis B and human immunodeficiency virus coinfection
Author(s) -
Malagnino Vincenzo,
Bottero Julie,
Miailhes Patrick,
LascouxCombe Caroline,
Girard PierreMarie,
Zoulim Fabien,
Lacombe Karine,
Boyd Anders
Publication year - 2019
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.25360
Subject(s) - hepatitis b virus , coinfection , medicine , fibrosis , genotype , gastroenterology , hepatitis b , orthohepadnavirus , immunology , hepadnaviridae , virology , virus , biology , gene , biochemistry
Infection with hepatitis B virus (HBV) genotype G has been associated with increased liver fibrosis levels compared with other genotypes in cross‐sectional studies, yet its role in fibrosis evolution remains to be established. Methods In this prospective cohort study, 158 human immunodeficiency virus (HIV)‐HBV coinfected patients had available HBV genotyping at baseline. Liver fibrosis was assessed at baseline and every 6 to 12 months by the FibroTest (BioPredictive, Paris, France). Risk factors for fibrosis regression (F3‐F4 to F0‐F1‐F2) and progression (F0‐F1‐F2 to F3‐F4) between baseline and end of follow‐up were evaluated. Results Most patients were male (88.6%) with a median age of 39 years. HBV genotype A was more prevalent compared with other HBV genotypes (62.7% vs D = 10.8%, E = 10.8%, and G = 15.8%). Patients were followed up for a median of 83 months (IQR = 37‐97). In the 43 (27.2%) patients with F3‐F4 baseline liver fibrosis, 7 (16.2%) regressed to F0‐F1‐F2 fibrosis at the last follow‐up visit. In the 115 (72.8%) with F0‐F1‐F2 fibrosis at baseline, 19 (16.5%) progressed to F3‐F4 fibrosis at last visit. In multivariable analysis, fibrosis progression was independently associated with older age ( P <0.005), baseline CD4+ cell count less than 350/mm 3 ( P <0.01), longer antiretroviral therapy duration ( P <0.03), and HBV genotype G infection (vs non‐G, P <0.01). When examining averages over time, the rate of FibroTest increase was faster in genotype G vs non‐G–infected patients with baseline F0‐F1‐F2 fibrosis ( P for interaction = 0.002). Conclusion In HIV‐HBV coinfected patients, HBV genotype G is an independent risk factor for liver fibrosis progression as determined by noninvasive markers. HBV genotype G–infected patients with low initial liver fibrosis levels may require more careful monitoring.