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).

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.

Inclusion criteria:

• Age > or = 45 years
• HIV-1 infection
• Number of T CD4+ lymphocytes before antiretroviral treatment < 350 cells/mm3
• Current number of T CD4+ lymphocytes > 200 cells / mm3 for 6 moths before inclusion
• Efficient and well tolerated antiretroviral treatment for more than 24 months
• HIV-1 viral load < 50 copies/ml for more than 24 months before inclusion
• Patient able to understand the nature, the objective and the methods of the study
• Patient having signed the informed consent
• Affiliation to French Social Security System

Exclusion criteria:

• Patient having a current evidence of II to IV rank of the ANRS scale clinical condition
• Patient having a current evidence of III to IV rank of the ANRS scale biological condition
• Patient has a current evidence of an active coinfection
• Patient has a current (active) diagnosis of acute hepatitis due to any cause. Patients with chronic hepatitis, including chronic hepatitis B and/or C, may enter the study as long as they have stable liver function tests and undetectable viral load of hepatitis B and/or C
• Patient has a cirrhosis
• Patient presents with a non infectious pathology that might give immune modifications
• Patient using immuno-modulator therapy or chemotherapy
• Patient is currently participating or has participated in a study (within the exclusion period defined by this study)
• Patient is pregnant or breastfeeding