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Title: APOBEC3G targets human T-cell leukemia virus type 1.
Authors: Sasada, Amane
Takaori-Kondo, Akifumi
Shirakawa, Kotaro  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-7469-1276 (unconfirmed)
Kobayashi, Masayuki  KAKEN_id
Abudu, Aierkin
Hishizawa, Masakatsu  KAKEN_id
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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