Smoking and HIV-1 infection are risk factors for COPD, which is among the most common comorbid conditions in people living with HIV-1. HIV-1 infection leads to persistent expansion of CD8+ T cells, and CD8+ T cell-mediated inflammation has been implicated in COPD pathogenesis. In this study, we investigated the effects of HIV-1 infection and smoking on T cell dynamics in patients at risk of COPD. Bronchoalveolar lavage (BAL), endobronchial brushings and blood from HIV-1 infected and uninfected non-smokers and smokers were analyzed by flow cytometry, and lungs were imaged by computed tomography. Chemokines were measured in BAL fluid, and CD8+ T cell chemotaxis in the presence of cigarette smoke extract was assessed in vitro. HIV-1 infection increased CD8+ T cells in the BAL, but this increase was abrogated by smoking. Smokers had reduced BAL levels of the T cell-recruiting chemokines CXCL10 and CCL5, and cigarette smoke extract inhibited CXCL10 and CCL5 production by macrophages and CD8+ T cell transmigration in vitro. In contrast to the BAL, CD8+ T cells in endobronchial brushings were increased in HIV-1 infected smokers, driven by an accumulation of effector memory T cells in the airway mucosa and an increase in tissue resident memory T cells. Mucosal CD8+ T cell numbers inversely correlated with lung aeration, suggesting an association with inflammation and remodeling. HIV-1 infection and smoking lead to retention of CD8+ T cells within the airway mucosa.