Abstract

This prospective study investigated the impact of lamivudine-containing antiretroviral therapy (ART) on HIV-positive patients in South Africa with baseline hepatitis B virus (HBV) infection. Follow-up samples from 56 HBV/HIV co-infected patients, 25 with occult HBV infection (OBI) and 31 with chronic HBV infection (CHB), were available for analysis. HBV viral loads were quantified at 6, 12, 18, and 24 months post-ART initiation by the COBAS TaqMan HBV Test 48 assay, and the HBV polymerase gene was amplified with an in-house nested polymerase chain reaction assay. During 24 months of lamivudine-based ART, 6 of 8 (75%) OBI and 4 of 6 (67%) CHB patients achieved undetectable levels of HBV DNA, while 2 patients had persistent HBV DNA levels ≥ 2 × 105 despite lamivudine-based ART for 24 months. HIV viremia was undetectable in all patients at 12 months, suggesting high adherence to ART. Several lamivudine-associated HBV resistance mutations, including L180M, A181T, M204I, and M204V, were observed. Sequence analysis also revealed a rare genotype G infection. While resource-limited settings may use lamivudine-based ART because of availability and low cost, antivirals with dual therapy against HBV and HIV (e.g., lamivudine and tenofovir) should always be recommended with the regular monitoring of HBV viremia levels.

Highlights

  • Human-immunodeficiency-virus (HIV) infection alters the course of the hepatitis B virus (HBV)disease by increasing the rate of chronicity, enhancing HBV replication, and accelerating liver-relatedViruses 2020, 12, 634; doi:10.3390/v12060634 www.mdpi.com/journal/virusesViruses 2020, 12, 634 morbidity and mortality [1,2,3,4,5,6,7]

  • This study investigated the impact of a lamivudine-containing antiretroviral therapy (ART) regimen on HBV during management of HIV/acquired immunodeficiency syndrome (AIDS) patients in Pretoria, South Africa

  • Of the occult HBV infection (OBI) baseline samples, HBV DNA was undetectable in 12%

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Summary

Introduction

Human-immunodeficiency-virus (HIV) infection alters the course of the hepatitis B virus (HBV)disease by increasing the rate of chronicity, enhancing HBV replication, and accelerating liver-relatedViruses 2020, 12, 634; doi:10.3390/v12060634 www.mdpi.com/journal/virusesViruses 2020, 12, 634 morbidity and mortality [1,2,3,4,5,6,7]. Human-immunodeficiency-virus (HIV) infection alters the course of the hepatitis B virus (HBV). HBsAg prevalence in HIV-positive South African pregnant women ranges from 3.4% to 6.2% [10,11]. HBV prevalence in HIV-positive patients who have developed acquired immunodeficiency syndrome (AIDS) tends to be higher, with a study on South Africans initiating antiretroviral therapy (ART) reporting HBsAg, and HBV DNA prevalence of 22.9% and 40.6%, respectively [4]. While expanding HIV treatment programs, significant challenges remain when managing HBV/HIV coinfected patients [7,12,13]. The current Southern African ART guidelines recommend testing for HBsAg before initiating ART to ensure that HIV/HBV-coinfected patients are placed on an appropriate ART regimen containing drugs that are active against

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