title: Prevalence and clinical relevance of occult hepatitis B in the fibrosis progression and antiviral response to INF therapy in HIV-HCV-coinfected patients.
abstract: Occult hepatitis B virus (HBV) infection is diagnosed when HBc antibodies (HBcAb) and HBV DNA are detectable in serum while hepatitis B surface antigen (HBsAg) is not. This situation has been frequently described in patients with chronic hepatitis C virus (HCV) infection. The objective of this study was to evaluate the prevalence of occult hepatitis B in HIV-HCV-coinfected patients and its clinical relevance in liver histology and viral response after interferon therapy for HCV. A total of 238 HIV-HCV-infected patients,negative for HBsAg, were included. Serum samples were analyzed for the presence of HBV DNA and HBcAb.HBV DNA quantification was determined with the Cobas TaqMan HBV Test (detection limit 6 IU/ml). Data from liver biopsy and laboratory tests were also analyzed. HBcAb resulted in 142 (60%) patients, being the independent associated factors: male gender, previous history of intravenous drug use, age, CD4 count,and HAV antibody presence. Among 90 HBcAb patients that we could analyze, HBV DNA was positive in 15 (16.7% of occult hepatitis B infection in this group, and 6.3% in the whole HIV-HCV cohort studied). No baseline factors, liver histology, or HCV therapy response were related to the presence of HBV DNA. We found that occult hepatitis B is a frequent condition present in at least 6.3% of our HCV-HIV patients and in more than 16% of those with HBcAb. Despite the high prevalence, this phenomenon does not seem to affect the clinical evolution of chronic hepatitis C or modify the viral response to interferon-based HCV therapies
authors.affiliation: Infectious Diseases Unit, Hospital Clinic, Villarroel, 170, Barcelona, Spain. mlaguno@clinic.ub.es
authors.forename: Montserrat
authors.initials: M
authors.lastname: Laguno
authors.forename: Maria
authors.initials: M
authors.lastname: Larrousse
authors.forename: José Luis
authors.initials: JL
authors.lastname: Blanco
authors.forename: Agathe
authors.initials: A
authors.lastname: Leon
authors.forename: Ana
authors.initials: A
authors.lastname: Milinkovic
authors.forename: Maria
authors.initials: M
authors.lastname: Martínez-Rebozler
authors.forename: Montserrat
authors.initials: M
authors.lastname: Loncá
authors.forename: Esteban
authors.initials: E
authors.lastname: Martinez
authors.forename: Jose Maria
authors.initials: JM
authors.lastname: Sanchez-Tapias
authors.forename: Elisa
authors.initials: E
authors.lastname: de Lazzari
authors.forename: José Maria
authors.initials: JM
authors.lastname: Gatell
authors.forename: Josep
authors.initials: J
authors.lastname: Costa
authors.forename: Josep
authors.initials: J
authors.lastname: Mallolas
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000494:pharmacology*; D001706:Biopsy; D015331:Cohort Studies; D015897:Comorbidity; D004279:DNA, Viral / Q000097:blood*; D018450:Disease Progression; D005260:Female; D006678:HIV; D015658:HIV Infections / Q000188:drug therapy; D006508:Hepatitis Antibodies / Q000097:blood*; D006509:Hepatitis B / Q000097:blood / Q000453:epidemiology* / Q000473:pathology*; D006512:Hepatitis B Core Antigens / Q000276:immunology*; D006514:Hepatitis B Surface Antigens / Q000097:blood; D006515:Hepatitis B virus / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification; D019698:Hepatitis C, Chronic / Q000188:drug therapy*; D006801:Humans; D007372:Interferons / Q000627:therapeutic use*; D008099:Liver / Q000473:pathology; D008103:Liver Cirrhosis / Q000175:diagnosis*; D008297:Male; D015995:Prevalence; D012189:Retrospective Studies; D013030:Spain / Q000453:epidemiology; D016896:Treatment Outcome
chemical_list: D000998:Antiviral Agents; D004279:DNA, Viral; D006508:Hepatitis Antibodies; D006512:Hepatitis B Core Antigens; D006514:Hepatitis B Surface Antigens; D007372:Interferons