Proviral HIV-1 DNA was defective in 26% of patients (n = 44): 24% contained in-frame stop codons (nonsense mutations) and 4% contained single nucleotide deletions (frameshift mutations). The median (IQR) total number of resistance mutations in both RT and PR among the 121 patients was 17 (15, 19) and 13 (8, 17) for HIV-1 RNA and DNA, respectively (P < 0.001). The respective median (IQR) number of resistance mutations for HIV-1 RNA and DNA

was 5 (5, 6) and 4 (2, 5) for NRTIs, 2 (1, 2) and 1 (0, 2) for NNRTIs, and 10 (8, 12) and 8 (3, 12) for PIs, respectively. The number of resistance mutations for each drug class was significantly lower in DNA than in RNA (P < 0.001). Figure 1 shows the frequencies of HIV-1 RNA and DNA mutations for the three drug classes. NRTI resistance mutations among the 128 RT available sequences were 20% more frequent in RNA than in DNA at codons M41L, D67N, L74V, M184V, L210W and find more T215Y/F. Only the mutation frequency at codon K70R was similar in RNA and DNA (31% and 34%, respectively). NNRTI

resistance mutations at codons K103N, Y181C and G190A/Q were 10% more frequent in RNA than in DNA. Among the 156 available PR sequences, major resistance mutations were 10% more frequent in RNA than in DNA at codons L33F/I/V, Gefitinib research buy M46I/L, I54M/L, V82A/C/F/G, I84V and L90M. In contrast, the mutation D30N was detected more frequently in DNA (10%) than in RNA (4%). Based on the RNA and DNA genotypes among the 121 patients, the median (IQR) numbers of drugs for which resistance and possible resistance were detected were, respectively, 12.5 (11.0, 13.5) and 8.8 (4.0, 10.5) for all antiretrovirals, PAK6 4.5 (4.0, 5.5) and 3.0 (1.0, 4.5) for NRTIs, 2.0 (2.0, 2.0) and 0.0 (0.0, 2.0) for NNRTIs, and 6.0 (5.0, 6.0) and 3.5 (0.0, 6.0) for PIs. The numbers of drugs for which resistance and possible resistance were detected were significantly lower in DNA than in RNA for all drug classes (P < 0.001). Figure 2 shows the percentage of patients with viruses resistant or possibly resistant to each member of the three therapeutic

classes. The percentage of patients with resistance or possible resistance was higher in the RNA genotype than in the DNA genotype for the majority of drugs, whatever the therapeutic class. The proportion with NRTI resistance among the 128 patients with available RT sequences ranged between 54 and 98% with RNA genotyping and between 35 and 76% with DNA genotyping. Resistance to at least one NRTI was detected by RNA genotyping but not by DNA genotyping in 63% of patients (81 of 128), and by DNA genotyping but not RNA genotyping in 13% of patients (17 of 128). NNRTI (efavirenz and nevirapine) resistance was found in 91–94% of patients by RNA genotyping and in 46–48% of patients by DNA genotyping. Resistance to at least one NNRTI was found by RNA but not by DNA genotyping in 47% of patients (60 of 128), and by DNA but not RNA genotyping in 1% of patients (one of 128).