title: Occult hepatitis B virus infection before and 1 year after start of HAART in HIV type 1-positive patients.
abstract: Occult hepatitis B virus (HBV) infection is diagnosed when HBc antibodies and HBV-DNA are detectable in serum while hepatitis B surface antigen (HBsAg) is not. The clinical relevance of this phenomenon in HIV-1 patients starting highly active antiretroviral therapy (HAART) is unknown. We followed 93 therapy naive HIV-1-infected adults who were anti-HBc positive, HBsAg and HBeAg negative, during first year of HAART. At baseline, HBV-DNA was quantified, and HBV genotype was determined in the HBV-DNA-positive patients by sequencing a part of the HBV genome. Four of 93 patients (4%) were HBV DNA positive at baseline. All four patients tested negative for HBV-DNA after 1 year. They all received lamivudine as part of their HAART. They had no clinically significant liver enzyme elevations (LEE) during the first year of HAART. Two of the patients had a genotype A, one genotype E, and in the fourth patient sequencing was not possible. In one patient we found significant mutations in the a determinant region of HBsAg, at positions 142 and 144. In our population of therapy-naive HIV-1-infected adults who were anti-HBc positive, we found occult HBV infection in 4% of the patients. We did not find an increased risk for LEE in our population of patients after the start of HAART. Our results illustrate that occult HBV infection is more a diagnostic than a clinical problem. It may be caused by very low levels of HBV replication, concurrent presence of HBsAg and anti-HBs, or mutations in the HBsAg a determinant.
authors.affiliation: Department of Internal Medicine, Division of Infectious Diseases, Tropical Medicine, and AIDS, National AIDS Trial and Evaluation Center (NATEC), Academic Medical Center, 1105 AZ Amsterdam, The Netherlands. K_pogany@amc.uva.nl
authors.forename: K
authors.initials: K
authors.lastname: Pogány
authors.forename: H L
authors.initials: HL
authors.lastname: Zaaijer
authors.forename: J M
authors.initials: JM
authors.lastname: Prins
authors.forename: F W
authors.initials: FW
authors.lastname: Wit
authors.forename: J M A
authors.initials: JM
authors.lastname: Lange
authors.forename: M G H M
authors.initials: MG
authors.lastname: Beld
mesh_terms: D000328:Adult; D019943:Amino Acid Substitution; D023241:Antiretroviral Therapy, Highly Active; D004279:DNA, Viral / Q000097:blood / Q000145:classification / Q000235:genetics; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy*; D006509:Hepatitis B / Q000150:complications*; D006510:Hepatitis B Antibodies / Q000097:blood; D006514:Hepatitis B Surface Antigens / Q000097:blood / Q000235:genetics; D006513:Hepatitis B e Antigens / Q000097:blood; D006515:Hepatitis B virus / Q000235:genetics / Q000276:immunology; D006801:Humans; D019259:Lamivudine / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D009154:Mutation; D017422:Sequence Analysis, DNA
chemical_list: D004279:DNA, Viral; D006510:Hepatitis B Antibodies; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens; D019259:Lamivudine