University hospital Montpellier
Montpellier, 34295, France
NCT Number: NCT02334943
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).
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Notify Me45 year and older
All sexes
Interventional
Not applicable
Montpellier, 34295, France
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.
Healthy volunteers accepted: Yes
Only the study team can determine whether someone qualifies for participation.
Inclusion criteria
Exclusion criteria
Blood test
Time frame: Infection of novo persistent the day of inclusion
Etiologic factors of persistent immune activation in treated HIV-1 infected patients (obstinacy of the infection of new cells T CD4 +, microbial translocation, active coinfection, immunosenescence, lymphopenia T CD4 +, deficit in lymphocytes Treg) on a day: the day of the inclusion
Time frame: Microbial translocation the day of inclusion
Microbial translocation (DNA bacterial plasma derivative)
Time frame: Diagnosis immunizing activation the day of inclusion
Activation T CD4 and T CD8, B, NK
Time frame: No immunological response to treatment the day of inclusion
Measurement of circulating CD4 +
Time frame: Renal Review the day of inclusion
Estimated glomerular filtration rate, Na / K / Cl / alkaline reserve, blood uric acid, typing with proteinuria, albuminuria, creatinine, phosphorus reabsorption, urine dipstick
Time frame: Bone balance the day of inclusion
Determination of Calcium and phosphate levels in fasting, PTH, TSH, 25hydroxy vitamin D, testosterone (male), estradiol (female)
Time frame: Metabolic syndrome assessment the day of inclusion
Metasting blood glucose, HbA1c, triglycerides, LDL cholesterol, HDL cholesterol
University Hospital, Montpellier
Other
Immune Activation in HIV-1 Infected Patients Under AntiRetroviral Treatment: Etiologic Factors, Forms and Potential Association With Chronic Comorbidities Unrelated to Immune Deficiency.
Acronym: ACTIVIH
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