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. Author manuscript; available in PMC: 2015 Mar 20.
Published in final edited form as: J Mol Biol. 2013 Nov 2;426(6):1220–1245. doi: 10.1016/j.jmb.2013.10.033

Figure 2. Mechanism of action of A3G during infection with HIV-1Δvif virions.

Figure 2

In virus producer cells, in the absence of a functional Vif protein, A3G (purple hexagon) is packaged into the viral particles. In the target cell, A3G exerts its antiviral activity by inhibiting reverse transcription, blocking integration, and inducing G-to-A hypermutation. In the hypermutation process, A3G mainly deaminates deoxycytidines in minus-strand DNA to deoxyuridines, which ultimately results in G-to-A hypermutation in the plus-strand DNA. Although hypermutated viral DNA may integrate into the host chromosomal DNA to form proviruses, they are largely defective.