 Immune Activation persists in HIV-1 infected patients despite efficient antiretroviral treatment. This immune activation is responsible for immune deficiency as well as for non-AIDS related comorbidities, such as non-alcoholic Fatty liver disease, metabolic syndrome or osteoporosis. The goal of this observational transversal multicentric study is to establish the etiologic factors of persistent immune activation in treated HIV-1 infected patients persistent de novo infection of T CD4 cells, microbial translocation, active coinfections, immunosenescence, T CD4 cells lymphopenia, Treg deficiency, its different forms activation of T CD4 cells, T CD8 cells, B cells, NK cells, monocytes, granulocytes, platelets, endothelial cells or general inflammation and the potential correlation between causes, forms of immune activation and emergent comorbidities kidney, bone or liver dysfunction, metabolic syndrome. These correlations could highlight physiopathologic mechanisms relating a specific cause of immune activation, activation of a specific subpopulation of immune cells and a comorbidity. Physiopathologic mechanisms could then be tested in vitro and lead into new therapeutic tracks of immune activation secondary to HIV-1 or to the natural ageing process. 