Human APOBEC3 Proteins, Retrovirus Restriction, and HIV Drug Resistance
Guylaine Haché 1, Louis M. Mansky 1, Reuben S. Harris 1
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*Correspondence: Guylaine Haché, Email not available
Abstract
Over 40 million people worldwide currently have HIV/AIDS. Many antiretroviral drugs have proveneffective, but drug-resistant HIV variants frequently emerge to thwart treatment efforts. Reverse transcriptionerrors undoubtedly contribute to drug resistance, but additional significant sources of viralgenetic variation are debatable. The human APOBEC3F and APOBEC3G proteins can potently inhibitretrovirus infection by a mechanism that involves retroviral cDNA cytosine deamination. Herewe review the current knowledge on the mechanism of APOBEC3-dependent retrovirus restrictionand discuss whether this innate host-defense system actively contributes to HIV genetic variation.
