Human APOBEC3 proteins, retrovirus restriction, and HIV drug resistance.
Over 40 million people worldwide currently have HIV/AIDS. Many antiretroviral drugs have proven effective, but drug-resistant HIV variants frequently emerge to thwart treatment efforts. Reverse transcription errors undoubtedly contribute to drug resistance, but additional significant sources of viral genetic variation are debatable. The human APOBEC3F and APOBEC3G proteins can potently inhibit retrovirus infection by a mechanism that involves retroviral cDNA cytosine deamination. Here we review the current knowledge on the mechanism of APOBEC3-dependent retrovirus restriction and discuss whether this innate host-defense system actively contributes to HIV genetic variation.
Haché
Guylaine
G
University of Minnesota, Department of Biochemistry, Molecular Biology and Biophysics, Minneapolis, MN 55455, USA.
Mansky
Louis M
LM
Harris
Reuben S
RS
D000071478:APOBEC Deaminases; D003564:Cytidine Deaminase; D043525:Cytosine Deaminase / Q000378:metabolism*; D024921:Drug Resistance, Multiple, Viral / Q000187:drug effects / Q000235:genetics*; D014644:Genetic Variation / Q000276:immunology; D006678:HIV / Q000187:drug effects*; D015658:HIV Infections / Q000188:drug therapy* / Q000235:genetics; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D012192:Retroviridae Infections / Q000517:prevention & control*
D043525:Cytosine Deaminase; D000071478:APOBEC Deaminases; C502889:APOBEC3 proteins, human; D003564:Cytidine Deaminase