Amini-Bavil-Olyaee Samad, Sheldon Julie, Lutz Thomas, Trautwein Christian, Tacke Frank
Department of Medicine III, University Hospital Aachen, Germany.
AIDS. 2009 Jan 14;23(2):268-72. doi: 10.1097/QAD.0b013e3283224316.
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.
在一名合并感染人类免疫缺陷病毒（HIV）和乙型肝炎病毒（HBV）的患者身上进行的分子分析显示，在含替诺福韦的治疗过程中出现了一种不寻常的HBV聚合酶突变（rtV191I），该突变同时导致HBsAg阴性介导的免疫逃逸以及对拉米夫定耐药，但对替诺福韦不耐药。表型分析显示突变体的复制能力受损，而前核心或核心启动子伴随突变（HBe抗原阴性）可恢复其复制能力。携带耐药和疫苗抗性的HBV突变体可能构成相当大的个体风险和公共卫生问题。
