Institut für Pathologie, Kliniken der Stadt Köln, Cologne, Germany.
J Clin Microbiol. 2010 Feb;48(2):631-4. doi: 10.1128/JCM.01073-09. Epub 2009 Dec 9.
Recently, we reported on three patients with chronic hepatitis B virus (HBV) infection for whom adefovir (ADF) therapy virologically failed, most likely due to a preexisting rtI233V HBV polymerase mutation. Here, we describe two further patients with chronic HBV infection who were found to develop the rtI233V mutation after initiation of ADF therapy. These patients represent the first cases known so far in which the rtI233V ADF resistance mutation evolved under persistent HBV replication during HBV therapy with ADF. Interestingly, one of the previously described patients, who was initially successfully switched from ADF to tenofovir (TDF) and became virologically suppressed subsequently, experienced a moderate but remarkable rebound of HBV viremia after switching from TDF to entecavir, due to the emergence of renal toxicity. Thus, we provide evidence for the selection and counterselection of the rtI233V ADF resistance mutation during antiviral therapy.
最近，我们报道了三例慢性乙型肝炎病毒（HBV）感染患者，他们的阿德福韦酯（ADF）治疗在病毒学上失败了，很可能是由于预先存在的 rtI233V HBV 聚合酶突变。在这里，我们描述了另外两例慢性 HBV 感染患者，他们在开始 ADF 治疗后发现出现了 rtI233V 突变。这些患者代表了迄今为止已知的在 ADF 治疗期间 HBV 复制持续存在的情况下，rtI233V ADF 耐药突变进化的首例病例。有趣的是，在最初成功从 ADF 转换为替诺福韦（TDF）并随后病毒学抑制的一名先前描述的患者中，由于出现肾毒性，在从 TDF 转换为恩替卡韦后，HBV 病毒血症出现中度但显著的反弹。因此，我们提供了抗病毒治疗期间选择和反向选择 rtI233V ADF 耐药突变的证据。
