For the no-ARDFP group, mean dPSS and iPSS

for the new ARV regimens at week 0 were 2.04 (SD = 1.41) and 2.41 (SD = 1.28), respectively. For the ARDFP patients, mean dPSS and iPSS measured at week 12 were 3.30 (SD = 1.38) and 3.49 (SD = 1.17), respectively. For the no-ARDFP patients, baseline (week 0) RC was not significantly correlated with log10 viral load (r = 0.046; P = 0.599) or CD4 cell count (r = −0.125; P = 0.157), but was significantly correlated with both dPSS and iPSS (r = 0.258; P = 0.003 and r = 0.223; P = 0.010, respectively). By design, none of the patients in either group had undetectable viral load at week 0. At week 12, one patient (0.7%) in the ARDFP group and 29 patients (26.7%) in the no-ARDFP group had viral load < 400 HIV-1 RNA copies/mL (P < 0.0001). The mean week 0 to week 12 CD4 cell count Protein Tyrosine Kinase inhibitor change was −29.6 (SD = 87.0) in the ARDFP patients, compared with +44.3 (SD = 91.2) in the no-ARDFP patients (P < 0.0001). Mean changes in log10 viral load were +0.36 (SD = 0.77) in the ARDFP patients and −0.88 (SD = 1.07) in the no-ARDFP patients (P < 0.0001). From week 0 to week 12, mean RC increased to a significantly greater extent in the ARDFP patients (+33.4%) compared with the no-ARDFP patients (+0.0%; P < 0.0001). This

above-mentioned difference in virological outcomes during treatment interruption (at week 12) was erased by week 24: 36 (25.2%) JQ1 datasheet and 32 (20.7%) patients in the ARDFP and no-ARDFP groups, respectively, had viral load < 400 copies/mL (P = 0.3519). Table 2 presents the predictive value of PSS for virological and immunological responses to salvage therapy among no-ARDFP patients. In univariate analysis, dPSS and iPSS were highly predictive of early virological response (week 0 to week 12 viral load

selleck screening library change) following initiation of salvage therapy in this group (general linear modelling F value = 5.41; P = 0.022 and F = 5.81; P = 0.018, respectively). dPSS, but not iPSS, remained predictive of virological responses at weeks 24 and 48 (Table 2). In multivariate analysis controlling for baseline RC, CD4 cell count and viral load, both dPSS and iPSS were strongly predictive of virological responses at week 12 (P = 0.002 and P = 0.003, respectively), week 24 (P < 0.001 and P = 0.003) and week 48 (P = 0.005 and P = 0.010). Neither dPSS nor iPSS was significantly correlated with immunological response in univariate or multivariate analyses. Week 0 RC was significantly correlated with week 12 CD4 cell count in the ARDFP patients (r = −0.215; P = 0.02), but not with week 0 to week 12 change in CD4 cell count (R = −0.010; P = 0.92) or viral load (R = −0.112; P = 0.26) during treatment interruption. RC at the end of ARDFP (week 12) did not predict early (week 12 to week 24) virological (P = 0.285) or immunological (P = 0.902) response to treatment resumption (Table 3). Neither dPSS nor iPSS was predictive of virological responses 12 weeks following resumption of ARV therapy (study week 24; P = 0.078 and P = 0.