Broad antiretroviral defence by human APOBEC3G through lethal editing of nascent reverse transcripts

By Bastien Mangeat, P. Turelli, G. Caron, M. Friedli, L. Perrin, Didier Trono. Nature, 2003

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Type I interferons in host defense. (2006, positive): “…APOBEC3G deaminates cytosine to uracil in reversetranscribed retroviral DNA, generating catastrophic mutations and rendering viral DNA susceptible to cleavage by uracil DNA glycosylase and apurinic-apyrimidinic (AP) endonuclease enzymes (Harris et al., 2003; Mangeat et al., 2003).”
Rates of evolutionary change in viruses: patterns and determinants (2008, background): “This enzymatic deamination is thought to be an intrinsic antiviral host defence mechanis”
Quasispecies Theory and the Behavior of RNA Viruses (2010, background): “Subsequent work demonstrated that APOBEC proteins could induce lethal mutagenesis of HIV through widespread deamination of the HIV genome during reverse transcription, and highly mutagenized HIV genomes with signatures of deamination have been observed in patients [51–56].”
Mechanisms of viral mutation (2016, background): “APOBEC3G was first shown to massively convert cytidines to uracils in the complementary HIV-1 DNA during or following reverse transcription [55] [56] [57] .”
The Evolution and Emergence of RNA Viruses (2009, background): “Of these, that involving the APOBEC3G (apolipoprotein B-editing catalytic polypeptide) gene—a remarkable anti-retroviral response of primates (Mangeat et al. 2003)—has generated the most interest.”