...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>World Journal of Gastroenterology >N-terminal and C-terminal cytosine deaminase domain of APOBEC3G inhibit hepatitis B virus replication.
【24h】

N-terminal and C-terminal cytosine deaminase domain of APOBEC3G inhibit hepatitis B virus replication.

机译：APOBEC3G的N端和C端胞嘧啶脱氨酶域抑制乙型肝炎病毒复制。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

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 showing that APOBEC3G andits N-terminal or C-terminal cytosine deaminase domain could suppress HBV replication in vitro and in vivo.
机译：目的：研究人载脂蛋白B mRNA编辑酶催化多肽3G（APOBEC3G）及其N端或C端胞嘧啶脱氨酶域介导的抗乙型肝炎病毒（HBV）体外和体内抗病毒活性的作用。方法：将哺乳动物肝癌细胞HepG2和HuH7与APOBEC3G及其N端或C端胞嘧啶脱氨酶域表达载体，1.3倍超长HBV DNA以及基因型B和C的线性单体HBV共转染。在体内研究中，使用了基于HBV载体的小鼠模型，其中通过大量尾静脉注射，将APOBEC3G及其N端或C端胞嘧啶脱氨酶域表达载体与1.3倍长的HBV DNA共递送。通过ELISA测定转染细胞的培养基中和小鼠血清中的乙型肝炎病毒表面抗原（HBsAg）和乙型肝炎病毒e抗原（HBeAg）的水平。通过Western印迹分析确定转染的细胞中乙型肝炎病毒核心抗原（HBcAg）的表达。通过Southern印迹分析检查与核心相关的HBV DNA。分别通过定量PCR和定量RT-PCR分析确定小鼠血清中的HBV DNA水平以及小鼠肝脏中的HBV核心相关RNA。结果：人APOBEC3G在HepG2细胞中具有剂量依赖性的抗HBV活性，并且对基因型B和C的抑制作用与基因型A相当。有趣的是，N端或C端胞嘧啶脱氨酶域单独使用也可以抑制HBV在HepG2细胞和Huh7细胞中的复制。与体外结果一致，用APOBEC3G及其N端治疗的小鼠血清中HBsAg水平显着降低，肝脏中血清HBV DNA和核心相关RNA水平降低50倍以上与对照相比，C1或C末端胞嘧啶脱氨酶结构域。结论：我们的发现可能提供了第一个证据，表明APOBEC3G及其N端或C端胞嘧啶脱氨酶结构域可在体内外抑制HBV复制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号