Molecular analysis of an HBsAg-negative hepatitis B virus mutant selected in a tenofovir-treated HIV-hepatitis B virus co-infected patient

AIDS. 2009 Jan 14;23(2):268-72. doi: 10.1097/QAD.0b013e3283224316.

Abstract

The molecular analysis performed in an HIV-hepatitis B virus (HBV) coinfected patient revealed selection of an unusual HBV polymerase mutation (rtV191I) during tenofovir-containing therapy, conferring simultaneously immune escape by HBsAg negativity and resistance to lamivudine but not tenofovir. Phenotypic analysis revealed impaired replicative capacity of mutants, which could be restored by concomitant precore or basal core promoter mutations (HBe-antigen-negativity). HBV mutants carrying drug and vaccine resistance may represent a considerable individual risk and public health concern.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenine / analogs & derivatives*
  • Adenine / therapeutic use
  • Adult
  • Antiviral Agents / therapeutic use*
  • Drug Resistance, Viral
  • Gene Products, pol / genetics
  • HIV Infections / complications
  • HIV Infections / drug therapy*
  • HIV Infections / virology
  • Hepatitis B Surface Antigens / analysis
  • Hepatitis B virus / drug effects
  • Hepatitis B virus / genetics*
  • Hepatitis B virus / physiology
  • Hepatitis B, Chronic / complications
  • Hepatitis B, Chronic / drug therapy*
  • Hepatitis B, Chronic / virology
  • Humans
  • Lamivudine / therapeutic use
  • Male
  • Mutation
  • Organophosphonates / therapeutic use*
  • Tenofovir
  • Virus Replication / genetics

Substances

  • Antiviral Agents
  • Gene Products, pol
  • Hepatitis B Surface Antigens
  • Organophosphonates
  • P protein, Hepatitis B virus
  • Lamivudine
  • Tenofovir
  • Adenine