Abstract |
The cytidine deaminase APOBEC3G (A3G) exerts a multifaceted antiviral effect against HIV-1 infection. First, A3G was shown to be able to terminate HIV infection by deaminating the cytosine residues to uracil in the minus strand of the viral DNA during reverse transcription. Also, a number of studies have indicated that A3G inhibits HIV-1 reverse transcription by a non-editing-mediated mechanism. However, the mechanism by which A3G directly disrupts HIV-1 reverse transcription is not fully understood. In the present study, by using a cell-based coimmunoprecipitation (Co-IP) assay, we detected the direct interaction between A3G and HIV-1 reverse transcriptase (RT) in produced viruses and in the cotransfected cells. The data also suggested that their interaction did not require viral genomic RNA bridging or other viral proteins. Additionally, a deletion analysis showed that the RT-binding region in A3G was located between amino acids 65 and 132. Overexpression of the RT-binding polypeptide A3G(65-132) was able to disrupt the interaction between wild-type A3G and RT, which consequently attenuated the anti-HIV effect of A3G on reverse transcription. Overall, this paper provides evidence for the physical and functional interaction between A3G and HIV-1 RT and demonstrates that this interaction plays an important role in the action of A3G against HIV-1 reverse transcription.
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Authors | Xiaoxia Wang, Zhujun Ao, Liyu Chen, Gary Kobinger, Jinyu Peng, Xiaojian Yao |
Journal | Journal of virology
(J Virol)
Vol. 86
Issue 7
Pg. 3777-86
(Apr 2012)
ISSN: 1098-5514 [Electronic] United States |
PMID | 22301159
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- HIV Reverse Transcriptase
- APOBEC-3G Deaminase
- APOBEC3G protein, human
- Cytidine Deaminase
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Topics |
- APOBEC-3G Deaminase
- Amino Acid Motifs
- Cell Line
- Cytidine Deaminase
(chemistry, genetics, metabolism)
- Down-Regulation
- HIV Infections
(enzymology, genetics, virology)
- HIV Reverse Transcriptase
(genetics, metabolism)
- HIV-1
(enzymology, genetics, physiology)
- Humans
- Protein Binding
- Virus Replication
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