Wild-type negative control reactions had ΔCt ranges of between 15 and 19 cycles for the K103N assay, and between 13 and >40 cycles for the Y181C assay. The M184V mutation was detected in one of 165 samples (0.6%; 95% CI 0–3.3%)

by population sequencing, and in 13 of 165 samples (7.9%; 95% CI 4.3–13.1%) by the minority method. Thus, the more sensitive assay increased detection of M184V 13-fold, which was statistically significant (P=0.0005; 95% CI 2–85-fold increase). Wild-type negative control reactions had a ΔCt range of between 16 and 17 cycles. These data are summarized graphically in Figure 1. Overall, 32 samples showed resistance by one or both methods. All the resistance-associated mutations selleck inhibitor detected with either assay type are summarized in Table 1. One hundred and thirty-three specimens which were revealed to be free of any major resistance mutations were negative in all three minority assays, and have been excluded for brevity. By standard genotyping, 21 of 165 samples (12.7%; 95% CI 8.1–18.8%) showed evidence of drug resistance in our study population, while using the combined approach, 32 of 165 samples (19.4%; 95% CI 13.7–26.3%) showed drug resistance. This increase of 45% was statistically significant (P=0.0020; 95% CI 15.2–83.7%). The majority of the difference was accounted Palbociclib cost for by additional

detection of M184V. Comparison of the effect by year showed that in 2003, using standard genotypic methods,

14 of 91 samples (15.4%; 95% CI 8.7–24.5%) had evidence of TDR, while using a combination of both methods this figure was 17 of 91 samples (18.7%; 95% CI 11.3–28.2%): an increase of 21.4% (95% CI −2.6 to 51.3%; P=0.25), which was not statistically significant. In 2006, using standard genotypic methods, eight of 74 samples (9.5%; 95% CI 3.9–18.5%) had evidence of TDR, while using a combination of both methods 15 of 74 samples (20.3%; 95% CI 11.8–31.2%) had evidence of TDR, i.e. an increase of 114.3% (95% CI 24.7–268.1%; P=0.0078) compared with 2003, which was highly statistically significant. There was also a 1.76-fold increase in detection of C59 purchase drug resistance mutations, using minority assays alone, between 2003 and 2006. This increase was not significant (P=0.057). We also compared the rate of drug resistance detection in those found to have recently acquired HIV infection and those found to have long-standing HIV infection, according to serological incidence profiling. Using the whole data set, 13 of 70 (18.5%; 95% CI 10.3-29.7%) recent HIV infections and 19 of 95 (20%; 95% CI 12.5–29.5%) chronic infections had evidence of drug resistance. The difference of 7.7% between recent and chronic infections was not statistically significant (95% CI −42.9 to 103.1%; P=0.8). In this population of homosexual men attending UK sexual health clinics, but in whom HIV infection was undiagnosed on arrival for this clinic visit, the overall prevalence of TDR was 12.