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Immunosuppressive Effects of Smoking and HIV-1 on the Development of Lung Disease.
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.
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.
Age
18 - 70 years
Sex
ALL
Healthy Volunteers
Yes
University of Colorado Denver
Aurora, Colorado, United States
Start Date
March 1, 2014
Primary Completion Date
July 1, 2019
Completion Date
December 1, 2019
Last Updated
December 18, 2019
210
ACTUAL participants
Lead Sponsor
University of Colorado, Denver
NCT07071623
NCT01875588
Data Source & Attribution
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