Immunosuppressive Effects of Smoking and HIV-1 on the Development of Lung Disease
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|ClinicalTrials.gov Identifier: NCT02058719|
Recruitment Status : Recruiting
First Posted : February 10, 2014
Last Update Posted : August 31, 2017
This study plans to learn more about pulmonary complications of human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS). Even though antiretroviral therapy (ART) has dramatically decreased the number of opportunistic infections and deaths in HIV infected patients, pulmonary complications (including chronic obstructive pulmonary disease (COPD) development and pneumonias resulting in decreased lung function) of HIV/AIDS continue to be a major cause of morbidity and mortality in this population. The mechanisms underlying the increased risk of COPD and decreased lung function in HIV infected individuals is not well understand and needs to be studied.
The investigators hypothesize that the immunoregulatory consequences and immunosuppressive lung milieu secondary to HIV and cigarette smoke combine to increase the risk of lung infection and injury in HIV infected smokers, hastening the development of COPD. The mechanisms will be directly tested using blood and bronchial alveolar lavage (BAL) cells from smokers and nonsmokers with and without HIV infection.
|Condition or disease|
|HIV Smoking COPD|
The first component of this study will be a longitudinal, prospective, 24 weeks study of the effects of HIV-1 infection on innate and acquired immunity in the lung (Cohort A). The second component of this study will be a cross-sectional, case-control study of lung function and immune dysregulation of HIV-1 infected persons on long-term ART (Cohort B).
Cohort A will consist of 120 subjects, stratified by HIV-1 and smoking status
Cohort B will consist of 90 subjects stratified by chronic obstructive pulmonary disease (COPD) and HIV-1 infection.
|Study Type :||Observational|
|Estimated Enrollment :||210 participants|
|Official Title:||Immunosuppressive Effects of Smoking and HIV-1 on the Development of Lung Disease.|
|Actual Study Start Date :||March 2014|
|Estimated Primary Completion Date :||August 2018|
|Estimated Study Completion Date :||August 2018|
HIV positive smokers
HIV positive non-smokers
HIV negative smokers
HIV negative non-smokers
HIV positive with COPD
HIV positive without COPD (non-COPD)
HIV negative with COPD
- The change in immunoregulatory markers: PD-1 expression and interleukin (IL)-10 production by alveolar macrophages (AMs) from baseline to week 24. [ Time Frame: Baseline, Week 24 ]Evaluate the immunoregulatory change between HIV positive (smokers/non-smokers) and HIV negative (smokers/non-smokers)
- PD-1 expression and IL-10 production by AMs at baseline [ Time Frame: Baseline ]Evaluate the association of PD-1 expression and IL-10 production by AMs after long-term antiretroviral therapy (ART) with abnormal lung function and a COPD phenotype between HIV positive (with and without COPD) and HIV negative with COPD.
Biospecimen Retention: Samples Without DNA
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT02058719
|Contact: Thomas B. Campbell, MDfirstname.lastname@example.org|
|Contact: Christine Griesmer, RNemail@example.com|
|United States, Colorado|
|University of Colorado Denver||Recruiting|
|Aurora, Colorado, United States, 80045|
|Contact: Thomas B. Campbell, MD 303-724-4929 firstname.lastname@example.org|
|Principal Investigator: Thomas B. Campbell, MD|
|Principal Investigator: Andrew Fontenot, MD|
|Principal Investigator:||Thomas B. Campbell, MD||University of Colorado, Denver|