FIG 4.

The correlation between K65R and greater ETR phenotypic resistance is limited to viral genomes containing 3 or more ETR NNRTI resistance-associated mutations. Fold change resistance was evaluated based on the contribution of the number of NNRTI-associated mutations A98G, L100I/V, K101E/H/P, K103H/N/S/T, V106A/I/M, V108I, E138A/G/K/Q/R, V179D/E/F/L, Y181C/F/G/I/V/S, Y188C/F/H/L, G190A/C/E/Q/S/T/V, H221Y, P225H, F227C/L, M230I/L, K238N/T, Y318F, or N348I (i.e., those with resistance scores ≥10 for one or more NNRTI as reported by the Stanford HIV Drug Resistance Database v8.4) per sample with and without K65R. Samples were grouped based on having zero, one, two, three, or four or more NNRTI-associated mutations. Samples with zero NNRTI-associated mutations include the 12 treatment-naive individuals (i.e., control samples derived from the ARV treatment-naive individuals from South Africa) that were used as wild-type comparators in this study. Each group displays individual FC values for all samples in the category (boxes), samples without K65R (circles), and samples containing K65R (triangles). The dotted line indicates the ETR phenotypic resistance clinical cutoff of 2.9-FC. ETR FC between samples with and without K65R were compared with the Mann-Whitney U-Test.