Optimisation of Primary HIV1 Infection Treatment(ANRS 147 OPTIPRIM)
|HIV-1 Infections||Drug: raltegravir; maraviroc; darunavir; ritonavir; tenofovir/emtricitabine Drug: darunavir; ritonavir; emtricitabine/tenofovir||Phase 3|
|Study Design:||Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: None (Open Label)
Primary Purpose: Treatment
|Official Title:||Optimisation of Primary HIV1 Infection Treatment (ANRS 147 OPTIPRIM)|
- To compare the 24-month impact of maximized vs. conventional HAART- on HIV reservoirs, as assessed by cell-associated HIV-DNA levels, in patients with acute or primary HIV-1 infection [ Time Frame: 24 months ]
- Plasma HIV-RNA levels and proportion of patients with plasma viral load < 50 copies/ml at M12, M24 and M30 [ Time Frame: 30 months ]
- Plasma HIV-RNA levels and proportion of patients with plasma viral load < 5 copies/ml at M24 [ Time Frame: 24 months ]
- Changes in cell-associated HIV-DNA between baseline and M24 [ Time Frame: 24 Months ]
- Evolution of the CD4 and CD8 between D0 and M24 [ Time Frame: 24 months ]
- Tolerability of trial treatments [ Time Frame: 24 months ]
- Number and type of ARV mutations in virological failures and change in CCR5 tropism [ Time Frame: 24 Months ]
|Study Start Date:||April 2010|
|Study Completion Date:||December 2013|
|Primary Completion Date:||July 2013 (Final data collection date for primary outcome measure)|
Experimental: arm 1
darunavir, ritonavir, emtricitabine/tenofovir, maraviroc, raltegravir
Drug: raltegravir; maraviroc; darunavir; ritonavir; tenofovir/emtricitabine
raltegravir (Isentress®): 400 mg bid. maraviroc (Celsentri®): 150 mg bid. darunavir (Prezista®): 800 mg QD. ritonavir tablet (Norvir®): 100 mg QD. tenofovir/emtricitabine (Truvada®): one 245/200 mg tablet QD.
Active Comparator: arm 2
darunavir, ritonavir, emtricitabine/tenofovir
Drug: darunavir; ritonavir; emtricitabine/tenofovir
darunavir (Prezista®): 800 mg QD. ritonavir tablet (Norvir®): 100 mg QD. tenofovir/emtricitabine (Truvada®): one 245/200 mg tablet QD.
Primary HIV-1 infection is characterized by a phase of intense replication, with a quick dissemination and early changes in the immune system. During primary HIV-1 infection, damages to MALT and GALT promotes a chronic cell activation, which participates in a progressive decay of immune functions.
After HAART initiation, the magnitude and rapidity of cell-associated HIV-DNA decrease are significantly higher in patients with primary HIV-1 infection than in patients with chronic infection (Ngo Giang Huong, AIDS 2004).
We hypothesize that an early intervention at different levels of viral replication with potent and well-tolerated new drugs may have a greater impact on cell-associated HIV-DNA levels than conventional triple-drug HAART.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01033760
|Hôpital Gustave Dron|
|Tourcoing, France, 59208|
|Principal Investigator:||Antoine CHERET, PH||Tourcoing Hospital|
|Principal Investigator:||Caroline LASCOUX-COMBE, PH||Saint Louis Hospital, Paris|
|Study Chair:||Laurence MEYER, Professor||Methodologist, INSERM U1018|
|Principal Investigator:||Bruno HOEN, Professor||Saint Jacques Hospital, CHU Besançon|
|Principal Investigator:||Isabelle RAVAUX, PH||Conception Hospital, Marseille|
|Principal Investigator:||Christine ROUZIOUX, Professor||Virology Investigator, Necker Hospital Paris|
|Principal Investigator:||Alain VENET, PH||Immunology Investigator, INSERM U1012 Bicêtre|
|Principal Investigator:||Daniel OLIVE, Professor||Immunology Investigator, Cancerology Institut Marseille|
|Principal Investigator:||Gianfranco PANCINO, PH||Immunology Investigator, Pasteur Institut Paris|
|Principal Investigator:||Brigitte AUTRAN, Professor||Immunology Investiigator, INSERM U543 Paris|