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• W2000620255 abstract "The human cytidine deaminase APOBEC3G edits both nascent human immunodeficiency virus (HIV) and murine leukemia virus (MLV) reverse transcripts, resulting in loss of infectivity [1Harris 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 (1100) Google Scholar, 2Mangeat 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 (1200) Google Scholar, 3Mariani R. Chen D. Schröfelbauer B. Navarro F. König R. Bollman B. Münk 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 (709) Google Scholar, 4Sheehy 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 (1833) Google Scholar, 5Zhang 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 (897) Google Scholar]. The HIV Vif protein is able to protect both viruses from this innate restriction to infection. Here, we demonstrate that a number of other APOBEC family members from both humans and rodents can mediate anti-HIV effects, through cytidine deamination. Three of these, rat APOBEC1, mouse APOBEC3, and human APOBEC3B, are able to inhibit HIV infectivity even in the presence of Vif. Like APOBEC3G, human APOBEC3F preferentially restricts vif-deficient virus. Indeed, the mutation spectra and expression profile found for APOBEC3F indicate that this enzyme, together with APOBEC3G, accounts for the G to A hypermutation of proviruses described in HIV-infected individuals [6Vartanian J.P. Meyerhans A. Asjo B. Wain-Hobson S. Selection, recombination, and G->A hypermutation of human immunodeficiency virus type 1 genomes.J. Virol. 1991; 65: 1779-1788Crossref PubMed Google Scholar, 7Vartanian J.P. Sommer P. Wain-Hobson S. Death and the retrovirus.Trends Mol. Med. 2003; 9: 409-413Abstract Full Text Full Text PDF PubMed Scopus (30) Google Scholar, 8Janini 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]. Surprisingly, although MLV infectivity is acutely reduced by APOBEC3G, no other family member tested here had this effect. It is especially interesting that although both rodent APOBECs markedly diminish wild-type HIV infectivity, MLV is resistant to these proteins. This implies that MLV may have evolved to avoid deamination by mouse APOBEC3. Overall, our findings show that although APOBEC family members are highly related, they exhibit significantly distinct antiviral characteristics that may provide new insights into host-pathogen interactions." @default.
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• W2000620255 date "2004-08-01" @default.
• W2000620255 modified "2023-10-15" @default.
• W2000620255 title "Cytidine Deamination of Retroviral DNA by Diverse APOBEC Proteins" @default.
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• W2000620255 doi "https://doi.org/10.1016/j.cub.2004.06.057" @default.
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