| Autor: |
Imada Kazunori, Hishizawa Masakatsu, Abudu Aierkin, Kobayashi Masayuki, Shirakawa Kotaro, Takaori-Kondo Akifumi, Sasada Amane, Tanaka Yuetsu, Uchiyama Takashi |
| Jazyk: |
angličtina |
| Rok vydání: |
2005 |
| Předmět: |
|
| Zdroj: |
Retrovirology, Vol 2, Iss 1, p 32 (2005) |
| Druh dokumentu: |
article |
| ISSN: |
1742-4690 |
| DOI: |
10.1186/1742-4690-2-32 |
| Popis: |
Abstract Background Apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G) is a host cellular protein with a broad antiviral activity. It inhibits infectivitiy of a wide variety of retroviruses by deaminating deoxycytidine (dC) into deoxyuridine (dU) in newly synthesized minus strand DNA, resulting in G-to-A hypermutation of the viral plus strand DNA. To clarify the mechanism of its function, we have examined the antiviral activity of APOBEC3G on human T-cell leukemia virus type 1 (HTLV-1), the first identified human retrovirus. Results In this study, we have demonstrated that overexpressed as well as endogenous APOBEC3G were incorporated into HTLV-1 virions and that APOBEC3G inhibited the infection of HTLV-1. Interestingly, several inactive mutants of APOBEC3G also inhibited HTLV-1 and no G-to-A hypermutation was induced by APOBEC3G in HTLV-1 genome. Furthermore, we introduced the human immunodeficiency virus type 1 (HIV-1) vif gene into HTLV-1 producing cell line, MT-2, to antagonize APOBEC3G by reducing its intracellular expression and virion incorporation, which resulted in upregulation of the infectivity of produced viruses. Conclusion APOBEC3G is incorporated into HTLV-1 virions and inhibits the infection of HTLV-1 without exerting its cytidine deaminase activity. These results suggest that APOBEC3G might act on HTLV-1 through different mechanisms from that on HIV-1 and contribute to the unique features of HTLV-1 infection and transmission. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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