Mechanisms for hepatitis B virus replication and mutagenesis : investigations using virus-expressing mouse system.

我们利用体外和体内的乙肝病毒表达系统研究了乙肝病毒的复制和诱变。结果表明：1)HBVpreS/S蛋白可能不影响单个乙肝病毒感染细胞中的复制；2)干扰素-γ可能不在最初根除乙肝病毒中起作用；3)与暴发性肝衰竭相关的新型乙肝病毒突变被鉴定；4)从免疫耐受期到免疫活动期发生的乙肝病毒突变可能减少乙肝病毒的复制；5)前C区和前S2区突变可能支持拉米夫定耐药乙肝病毒的复制；6)V1753和C2189突变可能导致对阿德福韦的抗病毒效果增强；7)发现了对多个核苷酸(T)类似物具有耐药性的新的乙肝病毒突变。

We studied hepatitis B virus (HBV) replication and mutagenesis using in vitro and in vivo HBV-expressing systems. The findings showed that 1) HBV preS/S protein may not affect HBV replication in a single HBV-infected cell, that 2) interferon-γ may not play a role on the initial eradication of HBV, that 3) the novel type of HBV mutation associated with fulminant hepatic failure was identified, that 4) HBV mutations occurring from immunotolerant phase to immunoactive phase may reduce HBV replication, that 5) precore and preS2 mutations may support replication of lamivudine-resistant HBV, that 6) V1753 and C2189 mutations may result in the improved antiviral efficacy against adefovir, and that 7) the novel HBV mutation that confer resistance to multiple nucleos(t)ide analogs was identified.