In cigarette smokers that are HIV+, one of the most common HIV-associated non-AIDS conditions is the accelerated development of chronic obstructive pulmonary disease (COPD), a disorder associated with significant morbidity and mortality. Based on the knowledge that COPD in smokers starts in the small airway epithelium, this study is focused on examining the hypothesis that the accelerated development of COPD associated with HIV infection results, in part, from an interaction of HIV directly on the small airway epithelium or through infection of cellular components of the immune system, with mediators released by these immune cells evoking premature biologic aging of the small airway epithelium. By identifying the early events in the pathogenesis of the HIV-associated accelerated COPD in smokers, we aim to identify biologic targets to which pharmacologic therapies could be addressed.