Advances in the study of molecular mechanism of APOBEC3G anti-HIV-1.
- Author:
Bo FAN
1
;
Shan CEN
;
Jian-dong JIANG
Author Information
1. Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
- Publication Type:Journal Article
- MeSH:
APOBEC-3G Deaminase;
Amino Acid Substitution;
Anti-HIV Agents;
metabolism;
Cytidine Deaminase;
genetics;
metabolism;
Gene Expression;
HIV Infections;
metabolism;
HIV-1;
genetics;
physiology;
Humans;
Virus Replication;
vif Gene Products, Human Immunodeficiency Virus;
genetics;
metabolism
- From:
Acta Pharmaceutica Sinica
2008;43(7):678-682
- CountryChina
- Language:Chinese
-
Abstract:
Apolipoprotein B mRNA-editing enzyme catalytic polypeptide 3 protein G (APOBEC3G) is part of the innate immune system of host cells and has cytidine deaminase activity. It specifically incorporates into the virion during HIV-1 replication. The incorporation of APOBEC3G needs its interaction with HIV-1 Gag. In the HIV-1 reverse transcription process, APOBEC3G deaminates dC to dU in the first minus strand cDNA, and then induces extensive hypermutation in the viral genome. Besides deamination, APOBEC3G also inhibits HIV-1 by some kinds of non-deamination mechanisms which need to be further elucidated. HIV-1 Vif counteracts the activity of APOBEC3G by an ubiquitin-proteasome-mediated degradation of APOBEC3G. As a broad spectrum inhibitor of viruses, APOBEC3G also inhibits various retroviruses, retrotransposons and other viruses like HBV. Upregulating the expression of APOBEC3G or blocking the Vif-mediated degradation of APOBEC3G might be novel strategies to treat HIV-1 infection in the future.
