HIV/HBV and HIV/HCV coinfection, and outcomes following highly active antiretroviral therapy

Abstract

ObjectivesTo assess the prevalence and risk factors for HBV and HCV coinfection in the Australia HIV Observational Database (AHOD), and examine outcomes of HIV disease following initiation of highly active antiretroviral therapy (HAART).MethodsAnalyses were based on 2086 participants recruited to AHOD by September 2002. Of these, 1605 (77%) had been tested for HBV surface antigen, 1704 (82%) for anti‐HCV antibody and 1453 (70%) for both. Demographic and clinical predictors of HBV and HCV coinfection were examined. The impact of HBV and HCV coinfection on HIV disease progression was assessed by Kaplan‐Meier survival curves and Cox proportional hazard model of time to AIDS events and death.ResultsAmong those tested, prevalence of HBV surface antigen and HCV antibody were 6.3% and 13.1%, respectively (4.8% and 10.7%, respectively, among the entire cohort). In multivariate analyses, the only independent risk factor for HIV/HBV coinfection was coinfection with HCV. Independent risk factors for HIV/HCV coinfection were HIV exposure category (with people who reported injecting drug use [MSM & IDU, IDU only] or receipt of blood or blood products at markedly increased risk) and HBV coinfection. HIV disease outcomes following first initiation of a HAART regimen were similar for HIV/HBV and HIV/HCV coinfected patients compared with HIV‐only patients in terms of AIDS‐free survival and detectable HIV virus during the first 12 months. However, patients coinfected with HIV/HCV appeared to have a poorer response to HAART in terms of CD4 count changes, with a CD4 count increase of 32 cells/μL (95% CI 1–67) less than HIV‐only patients.ConclusionsCoinfection with HBV or HCV is relatively common among HIV‐infected participants in AHOD. HIV disease outcomes following HAART do not appear to be adversely affected by HBV/HCV coinfection, except for slightly poorer CD4 count responses in HIV/HCV coinfected patients.

Triple positivity of HBsAg, anti-HCV antibody, and HIV and their influence on CD4+ lymphocyte levels in the highly HIV infected population of Abeokuta, Nigeria

“…Studies previously have proposed that dual positivity of HIV/HBV or HIV/HCV and triple positivity HIV/HBV/HCV have dampened immune reaction to HAART likened with those with only HIV [40][41][42] . While others studies have reported some degrees of immune reinstatement in individuals with HIV/HBV or HIV/HCV dual-infection [42][43][44][45][46][47][48] . Management of either hepatitis virus is multifaceted because of pharmacokinetic interfaces with constituents of HAART regimens.…”

Role of CD4 Count in Immunity Development After Hepatitis A and B Vaccination Among HIV-Infected Patients: Kentucky, 2002-2007

“…13,[16][17][18][19] Only a limited number of studies have examined association between other comorbidities in relation to their effect on hepatitis vaccine efficacy among patients infected with HIV. 20 In reviewing the scientific literature related to drug and alcohol use in relation to CD4 counts, we reviewed 1 study reporting that persons using drugs or alcohol had statistically significant decreases in CD4 counts; however, no studies evaluated the effects of other substances on immunity development. 21 This analysis provides information for the medical community regarding HAV/HBV vaccination among patients living with HIV/AIDS.…”

Simplification with Fixed-Dose Tenofovir-Emtricitabine or Abacavir-Lamivudine in Treatment Experienced, Virologically Suppressed Adults with Hiv Infection: Combined Analysis of Two Randomised, Non-Inferiority Trials Bicombo and Steal

“…However, the estimated prevalence of these coinfections in the Spanish HIV population (37% and 20-50% respectively) is greater than in the Australian (6% and 13% respectively). [17][18][19] The primary limitation of BICOMBO and STEAL, and therefore this combined analysis, was the inclusion of participants who were not naïve to TDF and ABC. However stratification by baseline NRTI showed no significant interaction between baseline exposure to ABC/ TDF and randomised treatment for any outcome.…”