Effects of human immunodeficiency virus on pulmonary host defenses

The ability of a microorganism to establish pulmonary infection depends not only upon its pathogenicity, but also on its ability to overcome host defense mechanisms. The frequency of pulmonary infections in patients with the acquired immunodeficiency syndrome (AIDS) suggests that pulmonary host defenses are compromised. The defense capabilities of the upper and lower airways, which prevent the majority of infectious organisms from reaching the lungs in healthy individuals, are not well characterized in AIDS. In the lower respiratory tract, direct infection of pulmonary alveolar macrophages by the human immunodeficiency virus may alter clearance of microorganisms. It is also likely that soluble signals required to activate alveolar macrophages are deficient in AIDS. Peripheral T and B lymphocytes from AIDS patients do not respond to antigen normally, and the resultant defects in cellular and humoral immunity may impair defenses against a variety of pulmonary pathogens. The defective microbicidal function of polymorphonuclear leukocytes from AIDS patients, and reduced migration of blood leukocytes into the lungs, may result in an insufficient cellular response to an infectious challenge. As the multiple defects in pulmonary host defenses associated with AIDS become characterized more fully, effective interventions for prevention and treatment of AIDS-related pulmonary infections can be developed.