Background:  Relatively little is known about the role of genotypes in patients co-infected with human immunodeficiency virus (HIV) and hepatitis B virus (HBV). Here, we examined the prevalence and impact of genotype on liver fibrosis in the co-infected patients. 

Methods:  We determined the HBV genotype in 133 HIV and HBV surface antigen (HBsAg)-positive patients, by direct sequencing performed on the surface region of HBV genome. We quantified HBV-DNA titers using Versant® HBV 3.0 and determined hepatitis B e antigen (HBeAg) and anti-HBe titers (n = 82) by ADVIA®Centaur assay. Median time of follow-up was 35 months (0 to 110). A non-invasive biomarker (Fib-4) was used to assess fibrosis stage with the results dichotomized.

Results: Genotype G was found in 23/133 (17%) and Genotype A in 99/133 (74%) followed by genotypes D (5%, 7/133), F (1.5%, 2/133), and H (1.52%, 2/133). GenotypeG appears in mixture with other HBV genotypes confirmed by the presence of high HBeAg levels [13/15 (87%) HBeAg positive; median1000; range (0 to 1000)], undetectable anti-HBe [12/14 (86%) anti-HBe negative; (median 0; range (0 to 2)], and high HBV-DNA levels (median 8.0 log₁₀  (range 4.1 to 8.0) copies/mL). Genotype G was associated with more advanced fibrosis, 39% (7/18) than genotype A [1% (8/70)], P =0.03. African Americans [49% (65/133)] had a higher prevalence of mild fibrosis compared to non-African Americans [Caucasians: 36% (50/133); Hispanics: 11% (14/133); others: 3% (4/133)], P =0.02. Using logistic regression, genotype G, OR = 5.1, 95%CI 1.4 to 18.4, P =0.01), was associated with increased fibrosis whereas being African American was associated with milder fibrosis (OR = 0.18, 95%CI, 0.04 to 0.72, P =0.02). 

Conclusions:  HBV genotype G comprised 17% of co-infection patients, and appears to determine fibrosis progression in co-infected patients.