Viral Hepatitis
Copyright ©2006 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Dec 14, 2006; 12(46): 7488-7496
Published online Dec 14, 2006. doi: 10.3748/wjg.v12.i46.7488
N-terminal and C-terminal cytosine deaminase domain of APOBEC3G inhibit hepatitis B virus replication
Yan-Chang Lei, Yong-Jun Tian, Hong-Hui Ding, Bao-Ju Wang, Yan Yang, You-Hua Hao, Xi-Ping Zhao, Meng-Ji Lu, Fei-Li Gong, Dong-Liang Yang
Yan-Chang Lei, Hong-Hui Ding, Bao-Ju Wang, You-Hua Hao, Xi-Ping Zhao, Dong-Liang Yang, Division of Clinical Immunology, Department of Infectious Disease, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China
Yong-Jun Tian, Yan Yang, Dong-Liang Yang, Center of Experimental Medicine, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China
Meng-Ji Lu, Department of Microbiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China
Meng-Ji Lu, Institute of Virology, Medical School of Duisburg-Essen University, Essen, Germany
Fei-Li Gong, Department of Immunology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China
Author contributions: All authors contributed equally to the work.
Supported by the National Natural Science Foundation of China, No. 30271170 and 30571646, and the National Key Basic Research Program of China, No. 20014CB510008 and 2005CB522900
Correspondence to: Professor Dong-Liang Yang, Division of Clinical Immunology and Department of Infectious Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, Hubei Province, China. dlyang@tjh.tjmu.edu.cn
Telephone: +86-27-83662894 Fax: +86-27-83662894
Received: July 27, 2006
Revised: October 25, 2006
Accepted: November 3, 2006
Published online: December 14, 2006
Abstract

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 and its N-terminal or C-terminal cytosine deaminase domain could suppress HBV replication in vitro and in vivo.

Keywords: Cytosine deaminase domain; Apolipoprotein B mRNA-editing enzyme catalytic-polypeptide 3G; Hepatitis B virus; Antiviral therapy