A multicentre observational database analysis was carried out. Data for patients whose highly active antiretroviral therapy (HAART) regime had been unchanged for ≥ 6 months by 1 January 2008, whose first two PVL measurements of 2008 were < 40 copies/mL and who had at least five PVL measurements between 1 January 2008 and 31 December 2010 were extracted check details from a multicentre observational database of 4928 patients

receiving HAART. PVL assays used during this period had a detection threshold of 20 or 40 copies/mL. Undetectable PVL at baseline (BLPCRneg) was defined as PCRneg at the first two PVL determinations of 2008. Multivariable Cox regression analysis was performed to investigate factors associated with the occurrence of blips and VF, defined as two consecutive PVL measurements > 40 copies/mL. Of the 1957 patients included in the study (mean age 47 years; median antiretroviral exposure

10.3 years), 1312 had BLPCRneg. Outcome events included 322 blips and 139 VFs, with incidence rates being significantly lower in patients with BLPCRneg than in those with BLPCRpos [13.0% vs. 23.4% (P < 0.0001) and 5.1% vs. 11.2% (P < 0.0001), respectively]. In multivariable analysis, BLPCRneg was associated Selleckchem IDH inhibitor with a reduced risk of blips [hazard ratio (HR) 0.58; 95% confidence interval (CI) 0.47–0.73; P < 0.0001] and VF (HR 0.44; 95% CI 0.31–0.62; P < 0.0001). Patients with PCRneg had better virological outcomes than those with PVL < 40 copies/mL but detectable viraemia. This suggests that the ‘no-signal’ information provided by currently

commercially available HIV RNA quantification assays should be used routinely. “
“As a switch from chemokine (C-C motif) receptor 5 [CCR5 (R5)] to chemokine (C-X-C motif) receptor 4 [CXCR4 (X4)] HIV-1 tropism is associated with symptomatic and AIDS stages of infection, while chemokine receptor gene variants modify the tempo of HIV disease progression, we aimed to analyse the association between pretreatment HIV-1 tropism and chemokine polymorphisms known to restrict disease progression. V3 genotype tropism prediction was performed in a group of 221 treatment-naïve patients, with subsequent CCR5 Δ32 (rs333), Amobarbital CCR2 V64I (rs1799864), CCR5 promoter (−627 C/T; rs1799988) and CX3CR1 V249I (rs3732378) genotyping performed in 206 patients. Alleles with a protective effect were assigned positive values while risk alleles were assigned negative values to calculate genetic scores. χ2 tests, Mann−Whitney U-tests and logistic and linear regression models were used for statistical analyses. R5 tropism was found in 85.5% of patients (n = 189) using a false positive rate (FPR) of 5.75% and in 72.8% of patients (n = 161) using an FPR of 10%. A higher frequency of the 5.75% FPR predicted R5 tropism was associated with the CX3CR1 A allele (P = 0.027). Lower additive genetic scores were associated with an increased frequency of 5.75% FPR predicted R5 tropism (P = 0.