This was the sesion were most of the new data on randomized clinical trials was presented.

The ESPRIT and SILCAAT studies found no clinical or virologic benefit of IL-2, but did show a significant increase in CD4 cells compared to ART alone. In these studies, patients with >300 CD4 cells (ESPRIT) and 50-299 CD4 cells (SILCAAT) were randomized to receive IL-2 + ART or ART alone. In the present analysis of pooled data on 5,805 patients from both studies, the risk of CD4 change and OD/death, as determined by the latest CD4 cell count, were no different in study and control groups. The risk of death or AIDS based on the latest CD4 cell count was significantly greater in patients receiving IL-2 in patients with >300 CD4 cells/ml. Twice as many psychiatric events were seen in treated patients compared to controls, and ART adherence data were not presented.  

MERIT compared maraviroc (MVC) to efavirenz (EFV) with ZDV/3TC. The original analysis using the old trofile assay showed non non inferiority of Maraviroc. The 48 week results, with the use of an enhanced sensitivity (ES) second generation tropism assay  showed non inferiority of MVC. In the 96 week data on BID MVC in this presentation, the ES tropism assay was again used, and no significant difference was seen between groups in patients with VL<50 c/ml (MVC 58.8% by ITT and 60.5% by TLOVR) and EFV (62.7% and 60.7, respectively). By the TLOVR analysis, the non-inferiority criteria for MVC compared to EFV were met; however, there were twice as many discontinuations due to virologic failure in the MVC arm (39) compared to EFV (18). CD4 increase was greater with MVC (224 cells/ml) than EFV (191 cells/ml). No new adverse events and no differences in OIs were seen; overall, 56 (18.5%) EFV patients discontinued drug due to adverse events, compared to 22 (6%) MVC patients. Lipid outcomes favored MVC, with more patients on EFV exceeding NCEP thresholds for total cholesterol and LDL cholesterol. The authors concluded that MVC was a viable option as initial therapy in R5-tropic patients. 

Min presented the results of an initial phase I mono-therapy study of S/GSK1349572, a novel integrase strand transfer inhibitor, in 35 HIV-1 infected naïve patients in doses of 2, 10, and 50mg once daily compared to placebo. The half life is 15 hours, with once daily dosing anticipated, and narrow variability in drug levels at each dose. The mean viral load decline at 11 days was 1.51-2.46 logs. 70% of patients in the 50mg dose group achieved an undetectable viral load. No phenotypic resistance was observed, nor were raltegravir or elvitegravir inhibitor mutations seen. The drug is entering phase IIb clinical trials. 

The STALWART study compared IL-2 alone; IL-2 together with pericycle antiretroviral therapy, consisting of a PI-inclusive regimen for 14 days (cycle 1) or 3 days (other cycles) prior to the IL2 administration, 5 days during the cycle, and 2 days after the cycle; and a control arm of no therapy in patients with CD4 counts >350.  The study was halted after the negative results of the ESPRIT and SILCAAT studies were announced.  There were greater increases in CD4+ counts in the IL-2 groups (+114  and +110 cells for 1L-2 and IL+ART) compared to -22 cells for the control arm (p<0.001). However, there were more possible HIV-related complications in the IL-2 arms (5 events in IL-2, 6 events in IL2+ART) compared to the control arm (1 event).  There were no differences in changes in viral loads when excluding subjects in the control arm who initiated ART, suggesting that the increase in CD4+ counts did not provide more fuel for HIV replication.  In addition, adverse events were greater in the IL2 arms (HR 2.6 and 4.05 for IL2 and IL+ART vs no IL2).  
 
Dr. Badal-Faeson presented the primary endpoints of a trial comparing LPV/r administered QD vs BID plus 2 NRTIs, selected on the basis of resistance testing, in patients failing therapy on an NNRTI or PI inclusive regimen.  Characteristics of the study population included 34% women, 49% non-Caucasion, CD4 count of 254, viral load of 4.26 log, and prior treatment experience with NRTIs among 99.5% of subjects with NNRTIs among 84.3% of subjects and with PIs in 46.1% of subjects.  Discontinuation rates were 4.7% in the QD arm and 7.4% in the BID arm.  Adherence, as measured by MEMS caps at week 8 was 89.6% in the QD arm versus 84.5% in the BID arm  (p<0.001).  The proportion of subjects with viral load <50 c/mL was 55.3% in the QD arm and 51.8% in the BID arm (difference 3.5%; 95% CI -4.5, 11.5).  Response rates by number of baseline LPV-associated mutations suggested that subjects with <3 mutations were more likely to achieve a viral load <50 c/mL on the QD arm, though subjects with ≥3 mutations had better responses on the BID arm.  There were no differences in tolerability or lipid changes.  These data suggest that QD LPV/r is as effective as BID therapy in patients with limited PI resistance. 

The MONET trial randomized patients with virologic suppression on an NNRTI- or boosted PI-based regimen for >6 months, no prior resistance, and history of darunavir therapy to either DRV/r (800 mg/100 mg) + 2 NRTI (n=129) or DRV/r alone (n=127). The primary endpoint was the proportion with a VL<50 at week 48 by TLOVR or changing therapy, except for reasons of switch of NRTI for tolerability.  Subjects were mostly male (80%) and White (91%) with a median CD4 count of 575, and a history of 6.4-7.4 years of therapy.  By the per protocol analysis (excluding subjects with major protocol violations, n=10), the percent of subjects with a viral load <50 c/mL was 87.8% of subjects on three-drug therapy and 86.2% of subjects on DRV/r alone (difference =-1.6, lower end of the 95% CI: -10.1).  There were more blips in patients on DRV/r alone, but PI mutations were rare, occurring in only one subject in each arm.  In addition, 10/11 subjects with quantifiable viral loads intensified therapy with NRTIs and achieved a viral load <50 c/mL at their last visit.  There was no difference in grade 2-4 adverse events or laboratory abnormalities.