HIV infection is suppressed but not cured by Anti-Retroviral Therapy (ART). This is due to the establishment of a viral reservoir that is responsible for the persistence of low levels of plasma viremia in patients under ART. Viral rebound is observed immediately after ART interruption. HIV persistence may arise from ongoing residual virus replication and/or from latentlyinfected cells in which long-lived resting memory CD4+ T cells harbouring transcriptionally silent provirus represent the largest pool in the blood. Addressing the source of HIV persistence is required to achieve a cure for HIV. We will discuss our recent data showing that CD32a is marker of HIV persistent CD4 T cell.