Immune Activation in HIV-1 Infected Patients Under AntiRetroviral Treatment

Not Applicable

Completed

• Conditions: Immune Deficiency; Activation of Latent Virus; HIV-related Gut Disease - Cause Unknown; Other Diagnoses, Comorbidities, and Complications

• Registration Number: NCT02334943
• Lead Sponsor: University Hospital, Montpellier

Brief Summary

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).

Detailed Description

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.

Study Timeline

• Study First Submitted: 2014-07-22
• Study First Submitted QC: 2015-01-06
• Study First Posted: 2015-01-08
• Study Start: 2015-03
• Primary Completion: 2015-03
• Study Completion: 2015-03
• Status Verified: 2015-11
• Last Update Submitted: 2015-11-19
• Last Update Posted: 2015-11-20

Recruitment & Eligibility

• Status: COMPLETED
• Sex: All
• Target Recruitment: 140

Inclusion Criteria

Not provided

Exclusion Criteria

Not provided

Study & Design

• Study Type: INTERVENTIONAL
• Study Design: PARALLEL

Primary Outcome Measures

Name	Time	Method
Infection of novo persistent	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

Secondary Outcome Measures

Name	Time	Method
Microbial translocation	Microbial translocation the day of inclusion	Microbial translocation (DNA bacterial plasma derivative)
Diagnosis immunizing activation	Diagnosis immunizing activation the day of inclusion	Activation T CD4 and T CD8, B, NK

Trial Locations

Locations (1)

University hospital Montpellier; 🇫🇷 Montpellier, France