Update: HIV infection and pulmonary host defenses

Infection with the human immunodeficiency virus (HIV) produces profound alterations in host defense mechanisms throughout the respiratory tract. The extent of alteration of specific defenses varies with the stage or duration of HIV infection in the host. In the upper respiratory tract, HIV-infected individuals have decreased concentrations of salivary immunoglobulin A, which may predispose to colonization of the oropharynx with pathogenic microorganisms. In the lower respiratory tract, host defenses are provided by alveolar macrophages, lymphocytes, and polymorphonuclear leukocytes. Alveolar macrophages can be chronically infected with HIV, and demonstrate a number of compromised host defense functions. The HIV-infected host has a limited capacity to generate soluble signals necessary for activation of alveolar macrophages for microbial killing. CD4 lymphocytes, which are quantitatively depleted during HIV infection, also demonstrate qualitative defects. Proliferation of CD8 lymphocytes, directed against HIV-infected cells in the lung, is associated with the noninfectious pulmonary complications of acquired immunodeficiency syndrome. B lymphocytes from HIV-infected persons show deficient production of opsonizing antibodies, which may predispose to bacterial pneumonias. Defective responses of polymorphonuclear leukocytes in the lung are also likely to contribute to impaired host responses. Collectively, these multiple defects in the defense mechanisms of the respiratory tract explain the unique susceptibility of the HIV-infected host for opportunistic pulmonary infections.