Fig. 4.

HIV-1 Vif mutants induce accumulation of 3TC-resistant proviruses. Forty-three percent (29/67) of the clones derived from PBMC infections with partially defective Vif mutants (K22E, E45G), but none of the clones derived from the Vif WT infections carry resistance-associated mutations in RT. (A) Proviruses carrying M184M (WT RT, open symbols, n = 88) and M184I (3TC-resistant, closed symbols, n = 44) display a range of deamination events. M184V was never detected. The mean number of G-to-A mutations in GG/GA dinucleotide context per infection is depicted by a horizontal line. (B) Correlation between the degree of deamination of Vif mutants (G-to-A mutations in GG/GA dinucleotide context) and stop codons in all clones (n = 73). Forty-three of these clones encoded M184I. The data from the three different PBMC donors were combined. R² denotes the goodness of fit.