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• W2056832684 abstract "APOBEC3G (CEM15 [1Sheehy A.M. Gaddis N.C. Choi J.D. Malim M.H. Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein.Nature. 2002; 418: 646-650Crossref PubMed Scopus (1849) Google Scholar]) deaminates cytosine to uracil in nascent retroviral cDNA [2Harris R.S. Bishop K.N. Sheehy A.M. Craig H.M. Petersen-Mahrt S.K. Watt I.N. Neuberger M.S. Malim M.H. DNA deamination mediates innate immunity to retroviral infection.Cell. 2003; 113: 803-809Abstract Full Text Full Text PDF PubMed Scopus (1112) Google Scholar, 3Zhang H. Yang B. Pomerantz R.J. Zhang C. Arunachalam S.C. Gao L. The cytidine deaminase CEM15 induces hypermutation in newly synthesized HIV-1 DNA.Nature. 2003; 424: 94-98Crossref PubMed Scopus (904) Google Scholar, 4Mangeat B. Turelli P. Caron G. Friedli M. Perrin L. Trono D. Broad antiretroviral defence by human APOBEC3G through lethal editing of nascent reverse transcripts.Nature. 2003; 424: 99-103Crossref PubMed Scopus (1213) Google Scholar, 5Lecossier D. Bouchonnet F. Clavel F. Hance A.J. Hypermutation of HIV-1 DNA in the absence of the Vif protein.Science. 2003; 300: 1112Crossref PubMed Scopus (577) Google Scholar]. The potency of this cellular defense is evidenced by a dramatic reduction in viral infectivity and the occurrence of high frequencies of retroviral genomic-strand G → A transition mutations [2Harris R.S. Bishop K.N. Sheehy A.M. Craig H.M. Petersen-Mahrt S.K. Watt I.N. Neuberger M.S. Malim M.H. DNA deamination mediates innate immunity to retroviral infection.Cell. 2003; 113: 803-809Abstract Full Text Full Text PDF PubMed Scopus (1112) Google Scholar, 3Zhang H. Yang B. Pomerantz R.J. Zhang C. Arunachalam S.C. Gao L. The cytidine deaminase CEM15 induces hypermutation in newly synthesized HIV-1 DNA.Nature. 2003; 424: 94-98Crossref PubMed Scopus (904) Google Scholar, 4Mangeat B. Turelli P. Caron G. Friedli M. Perrin L. Trono D. Broad antiretroviral defence by human APOBEC3G through lethal editing of nascent reverse transcripts.Nature. 2003; 424: 99-103Crossref PubMed Scopus (1213) Google Scholar, 5Lecossier D. Bouchonnet F. Clavel F. Hance A.J. Hypermutation of HIV-1 DNA in the absence of the Vif protein.Science. 2003; 300: 1112Crossref PubMed Scopus (577) Google Scholar]. The overwhelming dinucleotide hypermutation preference of APOBEC3G acting upon a variety of model retroviral substrates is 5′-G → -G [2Harris R.S. Bishop K.N. Sheehy A.M. Craig H.M. Petersen-Mahrt S.K. Watt I.N. Neuberger M.S. Malim M.H. DNA deamination mediates innate immunity to retroviral infection.Cell. 2003; 113: 803-809Abstract Full Text Full Text PDF PubMed Scopus (1112) Google Scholar, 3Zhang H. Yang B. Pomerantz R.J. Zhang C. Arunachalam S.C. Gao L. The cytidine deaminase CEM15 induces hypermutation in newly synthesized HIV-1 DNA.Nature. 2003; 424: 94-98Crossref PubMed Scopus (904) Google Scholar, 4Mangeat B. Turelli P. Caron G. Friedli M. Perrin L. Trono D. Broad antiretroviral defence by human APOBEC3G through lethal editing of nascent reverse transcripts.Nature. 2003; 424: 99-103Crossref PubMed Scopus (1213) Google Scholar, 6Yu Q. Konig R. Pillai S. Chiles K. Kearney M. Palmer S. Richman D. Coffin J.M. Landau N.R. Single-strand specificity of APOBEC3G accounts for minus-strand deamination of the HIV genome.Nat. Struct. Mol. Biol. 2004; 11: 435-442Crossref PubMed Scopus (493) Google Scholar, 7Mariani R. Chen D. Schrofelbauer B. Navarro F. Konig R. Bollman B. Munk C. Nymark-McMahon H. Landau N.R. Species-specific exclusion of APOBEC3G from HIV-1 virions by Vif.Cell. 2003; 114: 21-31Abstract Full Text Full Text PDF PubMed Scopus (761) Google Scholar, 8Shindo K. Takaori-Kondo A. Kobayashi M. Abudu A. Fukunaga K. Uchiyama T. The enzymatic activity of CEM15/Apobec-3G is essential for the regulation of the infectivity of HIV-1 virion but not a sole determinant of its antiviral activity.J. Biol. Chem. 2003; 278: 44412-44416Crossref PubMed Scopus (163) Google Scholar]. However, a distinct 5′-A → -A bias, which is difficult to attribute to APOBEC3G alone [9Beale R.C. Petersen-Mahrt S.K. Watt I.N. Harris R.S. Rada C. Neuberger M.S. Comparison of the differential context-dependence of DNA deamination by APOBEC enzymes correlation with mutation spectra in vivo.J. Mol. Biol. 2004; 337: 585-596Crossref PubMed Scopus (278) Google Scholar], prevails in HIV-1 sequences derived from infected individuals (e.g., [10Janini M. Rogers M. Birx D.R. McCutchan F.E. Human immunodeficiency virus type 1 DNA sequences genetically damaged by hypermutation are often abundant in patient peripheral blood mononuclear cells and may be generated during near-simultaneous infection and activation of CD4(+) T cells.J. Virol. 2001; 75: 7973-7986Crossref PubMed Scopus (159) Google Scholar]). Here, we show that APOBEC3F is also a potent retroviral restrictor but that its activity, unlike that of APOBEC3G, is partially resistant to HIV-1 Vif and results in a clear 5′-A → -A retroviral hypermutation preference. This bias is also apparent in a bacterial mutation assay, suggesting that it is an intrinsic APOBEC3F property. Moreover, APOBEC3F and APOBEC3G appear to be coordinately expressed in a wide range of human tissues and are independently able to inhibit retroviral infection. Thus, APOBEC3F and APOBEC3G are likely to function alongside one another in the provision of an innate immune defense, with APOBEC3F functioning as the major contributor to HIV-1 hypermutation in vivo." @default.
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• W2056832684 title "APOBEC3F Properties and Hypermutation Preferences Indicate Activity against HIV-1 In Vivo" @default.
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• W2056832684 doi "https://doi.org/10.1016/j.cub.2004.06.050" @default.
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