Turning up the volume on mutational pressure: Is more of a good thing always better? (A case study of HIV-1 Vif and APOBEC3)

Table 1 Observed APOBEC3-induced mutations at recognized HIV-1 RT resistance sites^a

HIV-1 RT Resistance Position	Wildtype Codon	APOBEC3G Target	APOBEC3F Target	Observed Mutant Codon	Mutant Frequency
M41 [NRTI]	ATG(G)	+	-	ATA	0.7
D67 [NRTI]	GAC	-	+	na	0
Q151 [NRTI]	CAG(G)	+	-	CAA×	0.5
M184 [NRTI]	ATG(G)	+	-	ATA*	0.6
L210 [NRTI]	TTG(A)	-	+	TTA×	0.1
E138 [NNRTI]	GAG(A)	-	+	AAG*	0.3
G190 [NNRTI]	GGA	+	+	AGA	0.5
M230 [NNRTI]	ATG(G)	+	-	ATA	0.7

^aAll available hypermutant HIV-1 subtype B reverse transcriptase sequences in the Los Alamos HIV Sequence Database [40] were analyzed (1 sequence sampled per individual, 10 total). Listed resistance positions are potential targets of APOBEC3G and/or APOBEC3F. Class of antiretroviral resistance listed in brackets (NRTI = nucleoside RT inhibitor, NNRTI = non-nucleoside RT inhibitor) [51]. Nucleotides in parentheses are immediately downstream of codons involved in antiretroviral resistance, and are included in the APOBEC3 dinucleotide target motifs. x = synonymous (silent) mutation, * = canonical resistance codon.

ISSN: 1742-4690