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Title: | APOBEC3G targets human T-cell leukemia virus type 1. |
Authors: | Sasada, Amane Takaori-Kondo, Akifumi Shirakawa, Kotaro https://orcid.org/0000-0002-7469-1276 (unconfirmed) Kobayashi, Masayuki Abudu, Aierkin Hishizawa, Masakatsu Imada, Kazunori Tanaka, Yuetsu Uchiyama, Takashi |
Author's alias: | 高折, 晃史 |
Issue Date: | 19-May-2005 |
Publisher: | BioMed Central Ltd. |
Journal title: | Retrovirology |
Volume: | 2 |
Thesis number: | 32 |
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. |
Rights: | © 2005 Sasada et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
URI: | http://hdl.handle.net/2433/159705 |
DOI(Published Version): | 10.1186/1742-4690-2-32 |
PubMed ID: | 15943885 |
Appears in Collections: | Journal Articles |
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