836    

Background: Chronic hepatitis B virus (HBV) infection affects 8% to 11% of patients with HIV infection. Antiretroviral medications with activity against both viruses, such as emtricitabine (FTC), may provide benefit by controlling both HIV and HBV replication.

Methods:  Patients were enrolled in one of three, 48-week studies evaluating emtricitabine as part of a triple drug regimen for the treatment of HIV infection. Regimens included FTC + didanosine + efavirenz (n = 286), FTC + stavudine + efavirenz or nevirapine (n = 234), and FTC + stavudine with either emivirine (an investigational non-nucleoside reverse transcriptase inhibitor) or abacavir (n = 564). Samples from patients shown to be HBsAg+ at baseline and exposed to >6 months of FTC with demonstrable HIV RNA suppression were evaluated for HBV DNA viral load and for genotypic findings. HBV DNA viral load analysis was performed on patient plasma using the Digene HBV Test Hybrid Capture II Assay with a lower limit of detection (LOD) of 4700 copies/mL. Genotypic analysis of the HBV polymerase was performed for baseline and week 48 samples that quantified >4700 copies/mL. 

Results:  We identified 39 HBsAg⁺ patients for analysis, with 24/39 (62%) having HBV DNA > 4700 copies/mL at baseline. For the 24 patients with detectable viremia, HBV viral load was determined every 12 weeks to week 48.  At baseline, the median HBV DNA was 8.68 log₁₀ copies/mL. Seventeen patients were available for evaluation at week 48; 14 of whom (82%) had a greater than 5 log₁₀ decrease in HBV DNA, or had HBV DNA below LOD at week 48.  Genotypic analysis of the HBV polymerase from the seven patients with detectable HBV DNA at week 48 showed that two had developed a mutation in the YMDD region (M204M/I) while none of the patients had developed the dual L180M/M204V mutations.  Overall, the proportion of co-infected patients below LOD and the incidence of new mutations in this population was not different when compared to a subgroup of chronic HBV infected patients treated with emtricitabine for 1 year (95% CIs for the difference between groups were -22%, 36% and -16%, 21%, respectively).

Conclusions: Emtricitabine, as a component of HAART, produced potent suppression of HBV DNA in treatment naïve, HBV co-infected patients as shown by a decrease in HBV DNA levels, the proportion of patients with HBV DNA levels below LOD and the low incidence of resistance associated mutations following 48 weeks of therapy.

Keywords: emtricitabine; hepatitis; resistance