APOBEC3G-mediated G-to-A hypermutation of the HIV-1 genome: the missing link in antiviral molecular mechanisms

APOBEC3G-mediated G-to-A hypermutation of the HIV-1 genome: the missing link in antiviral molecular mechanisms

Blog Article

APOBEC3G (A3G) is a member of the cellular polynucleotide cytidine deaminases, which catalyze the deamination of cytosine (dC) to uracil (dU) in single-stranded DNA.These enzymes potently inhibit the replication of a variety A2B Ford Pre-Amp of retroviruses and retrotransposons, including HIV-1.A3G is incorporated into vif-deficient HIV-1 virions and targets viral reverse transcripts, particularly minus-stranded DNA products, in newly infected cells.

It is well established that the enzymatic activity of A3G is closely correlated with the potential to greatly inhibit HIV-1 replication in the absence of Vif.However, the details of the axle fix underlying molecular mechanisms are not fully understood.One potential mechanism of A3G antiviral activity is that the A3G-dependent deamination may trigger degradation of the dU-containing reverse transcripts by cellular uracil DNA glycosylases (UDGs).

More recently, another mechanism has been suggested, in which the virion-incorporated A3G generates lethal levels of the G-to-A hypermutation in the viral DNA genome, thus potentially driving the viruses into error catastrophe mode.In this mini review article, we summarize the deaminase-dependent and deaminase-independent molecular mechanisms of A3G and discuss how A3G-mediated deamination is linked to antiviral mechanisms.