Obstructive lung disease and HIV/AIDS in the HAART era

Abstract

Early in the AIDS epidemic opportunistic lung infections, most notably Pneumocystis infection, dominated the clinical picture and were the most common cause of death in HIV-infected individuals. With the progressive development of effective antiretroviral treatments and prophylaxis against Pneumocystis, the prognosis in HIV/AIDS has improved dramatically with median survival now greater than a decade. However, lung infections from opportunistic, as well as typical bacterial pathogens remain a major cause of morbidity and are still the leading cause of death from HIV/AIDS. In addition, as the survival of infected individuals has increased, it is becoming apparent that other more-chronic lung diseases, including emphysema and cancer, are more common in these individuals. Although the mechanisms by which HIV/AIDS increases the risk of both infectious and noninfectious lung diseases are still being investigated, there is emerging evidence from clinical and experimental studies that HIV causes oxidant stress within the airways and that this may render the airway epithelium more susceptible to damage from environmental stresses, such as tobacco smoke. In parallel, there is intriguing evidence that colonization of the lower airways with Pneumocystis may promote chronic airway inflammation and destruction even when there is no clinical evidence of overt infection. Therefore, an important manifestation of HIV/AIDS, even in the HAART era, may be chronic oxidative stress and inflammation within the airways, rendering these individuals more susceptible to a wider range of lung diseases than previously seen early in the epidemic. This article focuses primarily on the emerging association between HIV/AIDS and chronic obstructive pulmonary disease, a clinical entity that includes emphysema and chronic bronchitis, and summarizes some of the recent clinical and experimental evidence that implicates HIV/AIDS in the HAART era as a potent risk factor for this common and disabling lung disease.