All our samples could be amplified and sequenced. The CRF02_AG subtype was identified in 72 of the 101 samples (71.3%). The distribution of other subtypes was as follows: eight CRF06_CPX (7.9%), six B (5.9%), four C (4%), three G (3%), two CRF09_CPX (2%), two CRF01_AE (2%), two A1 (2%), one CRF13_CPX (1) and one A2/CRF16_A2D find more (1%) (Fig. 1) Nucleoside reverse transcriptase inhibitor (NRTI), nonnucleoside reverse transcriptase inhibitor (NNRTI) and protease inhibitor (PI) mutations. Table 2 summarizes the drug resistance mutations observed in our cohort. Out of 101 patients, 10 patients had at least one mutation from one of the three drug classes,

with a clear impact on phenotypic susceptibility for the subtypes observed. This represents a prevalence of 9.9% (95% CI 6.9–12.9%). The prevalences of mutations associated with resistance to NRTIs, NNRTIs and PIs were 5% (95% CI 0.7–9.2%), 6% (95% CI 1.3–10.6%) and 0%, respectively. The most frequent resistance mutations were T215A/Y for NRTIs and K103N/T for NNRTIs. One patient harboured

three NRTI resistance mutations (M41L, M184V and T215Y) and one NNRTI mutation (K103N). This is the first reported case of multi-drug-resistant viral transmission in Mali. Other changes in the protease gene which have been associated with resistance to PIs in subtype B isolates were observed. These were the mutations L10I/V (found in 18.80% of patients) and L33F. The effect of these mutations on resistance is not clear for non-B subtypes and they may represent polymorphisms. If we take into consideration these mutations as potential resistance mutations, the prevalence of Fenbendazole primary selleck products resistance would increase to 28.70% (95% CI 19.89–37.53%). Phylogenetic analysis revealed that isolates with the 10I/V mutation were not

epidemiologically linked. We observed several polymorphisms in the C-terminal domain of the reverse transcriptase gene (amino acids 293–560). Recent studies have identified several mutations in this domain associated with resistance in subtype B, such as E312Q, G333E/D, G335D, N348I, A360I, V365I, T369I, A371V, A376S, T377L, E399D, L469T, Q509L and K558R [39–42]. In our study we observed four of these mutations, two of which had particularly high prevalences: G335D (prevalence 76.2%; 95% CI 67.9–84.5%), A371V (63.4%; 95% CI 54–72.8%), E399D (10.9%; 95% CI 4.8–17%) and G333E (1%; 95% CI 1–1.0%). There is little information about the effects of these mutations in the non-B subtype. We evaluated primary antiretroviral drug resistance in Bamako, Mali using samples collected between July 2007 and October 2008. Subtype analysis showed a high frequency of the recombinant form CRF02_AG, at 71.3% (Fig. 1). This result is consistent with a recent study conducted in Mali, which showed a frequency of 72% [7]. The frequency of this recombinant form was 75% in 2005 and 88% in 2002 [9]. There seems to have been a decline in the frequency of CRF02_AG over time.