中文摘要：

瞄准：调查人的 apolipoprotein B 编辑 mRNA enzymecatalytic 多肽 3G (APOBEC3G ) 和它的 N 终端或 C 终端 cytosine 的效果对在 vitro 并且在 vivo 的肝炎 B 病毒(HBV ) 的调停 deaminasedomain 的抗病毒的活动。方法: 哺乳动物的 hepatoma 房间 HepG2 和 HuH7 也是有 APOBEC3G 和它的 N 终端海怪终端 cytosine 脱氨基酶域表达式向量和第 1.3-fold-overleng HBV DNA 的 cotransfected 著名计算机生产厂商他遗传型 B 和 C 的线性 monomeric HBV。为在 vivo 学习，一个 HBV 基于向量的鼠标模型在在哪个 APOBEC3G 和它的 N 终端或 C 终端 cytosine，脱氨基酶域表达式向量经由大量的尾巴静脉注射与第 1.3-fold-overleng HBV DNA 被共同交付被使用。肝炎 B 病毒表面抗原(HBsAg ) 和在 transfected 房间的媒介并且在重量的单位的肝炎 B 病毒 e 抗原(HBeAg ) 的层次一 of 鼠标被 ELISA 决定。在 transfected 房间的肝炎 B 病毒核心抗原(HBcAg ) 的表示被西方的污点分析决定。联系核心的 HBV DNA 被南部的污点分析检验。在 theser 的 HBV DNA 的层次一象在老鼠的肝的 HBV 联系核心的 RNA 一样的 of 老鼠被 quantitativePCR 和量的 RT-PCR 分析分别地决定。结果：人的 APOBEC3G 在 HepG2 房间以一种剂量依赖者方式施加了 anti-HBVactivity，并且可比较的镇压效果作为遗传型 A 的在遗传型 B 和 C 上被观察。有趣地， N 终端或 C 终端 cytosinedeaminase 领域能也独自象 Huh7 房间一样在 HepG2 房间禁止 HBV 复制。与一致在 vitro 结果，在重量的单位的 HBsAg 的层次一of 老鼠戏剧性地被减少，与在浆液 HBV DNA 和联系核心的 RNAin 的层次的超过 50 次减少，老鼠的肝与 APOBEC3G 和它的N终端或C终端 cytosine 脱氨基酶领域当作了与控制相比。结论：我们的调查结果可能提供 APOBEC3G 和它的 N 终端或 C 终端 cytosine 脱氨基酶领域能压制的第一证据 howing 在 vitro 并且在 vivo 的 HBVreplication。

英文摘要：

AIM： To investigate the effect of human apolipoprotein B mRNA-editing enzyme catalytic-polypeptide 3G （APOBEC3G） and its N-terminal or C-terminal cytosine deaminase domain-mediated antiviral activity against hepatitis B virus （HBV） in vitro and in vivo. METHODS： The mammalian hepatoma cells HepG2 and HuH7 were cotransfected with APOBEC3G and its N-terminal or C-terminal cytosine deaminase domain expression vector and 1.3-fold-overlength HBV DNA as well as the linear monomeric HBV of genotype B and C. For in vivo study, an HBV vector-based mouse model was used in which APOBEC3G and its N-terminal or C-terminal cytosine deaminase domain expression vectors were co-delivered with 1.3-fold-overlength HBV DNA via high-volume tail vein injection. Levels of hepatitis B virus surface antigen （HBsAg） and hepatitis B virus e antigen （HBeAg） in the media of the transfected cells and in the sera of mice were determined by ELISA. The expression of hepatitis B virus core antigen （HBcAg） in the transfected cells was determined by Western blot analysis. Core-associated HBV DNA was examined by Southern blot analysis. Levels of HBV DNA in the sera of mice as well as HBV core-associated RNA in the liver of mice were determined by quantitative PCR and quantitative RT-PCR analysis, respectively. RESULTS： Human APOBEC3G exerted an anti-HBV activity in a dose-dependent manner in HepG2 cells, and comparable suppressive effects were observed on genotype B and C as that of genotype A. Interestingly, the N-terminal or C-terminal cytosine deaminase domain alone could also inhibit HBV replication in HepG2 cells as well as Huh7 cells. Consistent with in vitro results, the levels of HBsAg in the sera of mice were dramatically decreased, with more than 50 times decrease in the levels of serum HBV DNA and core-associated RNA in the liver of mice treated with APOBEC3G and its N-terminal or C-terminal cytosine deaminase domain as compared to the controls. CONCLUSION： Our findings provide probably the first evidence