Both COPD and HIV are associated with increased inflammasome activation, susceptibility to oxidative stress and persistent activation or dysfunction of lung immune cells(29). In addition to environmental risk factors such as smoking or biomass exposure, HIV likely leads to direct cytopathic effect or persistent immune activation which leads to inflammation and increased risk of COPD (22). Though high HIV viral load in plasma correlate with high levels of inflammatory cytokines, neither suppressive anti-retroviral therapy nor HIV viral load consistently correlate with the incidence or progression of COPD (21). The progression of HIV-related COPD correlate with elevated systemic markers of inflammation such as sCD14 and sCD163, which raises the possibility that these cells either serve as a site of HIV persistence or are activated by local tissue reservoirs that may not be adequately measured in the blood or BAL (3). It is postulated that HIV infection leads to abnormal immune responses in the airway that impacts the capacity of the lung to regulate response to environmental toxins such as cigarette and biomass smoke. Hence, even mild exposures to the noxious substances that are not clinically relevant in a HIV-negative individual may lead to the development or earlier progression of COPD amongst HIV positive individuals (21). 

COPD may progress more rapidly in patients with HIV, particularly in those that are currently smoking and have poorly controlled HIV. People with HIV may have a greater risk of COPD exacerbation compared to people without HIV (30).