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The main aim of this study was to determine whether HIV replication can be controlled following interruption of treatment started early in the course of infection (CD4+ >350 cells/μl and viral load <50 000 copies/ml), but not during the primary infection.Patients enrolled in a multicenter trial of treatment interruption (ANRS 116 SALTO) with CD4+ above 450 cells/μl and viral load below 400 copies/ml at treatment interruption were selected for this second analysis. We determined the proportion of patients whose plasma HIV-RNA load remained below 400 copies/ml during the first 12 months of treatment interruption, and baseline factors predictive of time to loss of viral control. Viral load rebound was defined as two successive values above 400 copies/ml, or as one value above 400 copies/ml, followed by treatment resumption.We studied 95 patients with a median CD4+ nadir of 382 cells/μl (340–492). At treatment interruption, the median CD4+ cell count and HIV-DNA load were 813/μl (695–988) and 206 copies/106 peripheral blood mononuclear cells (PBMCs) (53–556). Twelve months after treatment interruption, seven patients still had viral load below 400 copies/ml (Kaplan–Meier estimate 7.5%, 95% confidence interval 3.7–14.6), and four of them still had viral load below 400 copies/ml at 36 months. A multivariable Cox proportional-hazards model showed that time to loss of viral control was more shorter in patients with HIV-DNA at least 150 copies/106 PBMCs at treatment interruption (hazard ratio 2.1, 95% confidence interval 1.3–3.3, P = 0.002) than in those with HIV-DNA below 150 copies/106 PBMCs.Patients who have low HIV-DNA levels at antiretroviral treatment interruption are more likely to maintain viral control for long periods.