Failure of host defenses in human immunodeficiency virus

Abstract

Infection with human immunodeficiency virus (HIV) creates systemic immunosuppression but induces unique alteration of immune functions within lung tissue as well. Cells within the lung, particularly the alveolar macrophage, are important reservoirs of HIV infection. The body's immune response to HIV-infected lung cells creates a persistent inflammatory environment within the alveolar space, which compromises host responses to infectious pathogens. HIV infection alters mucociliary function as well as critical components of airway secretions. Within lung parenchyma, innate and adaptive immune responses to inhaled microorganisms are impaired, including neutrophil influx, lymphocyte responses, and humoral immunity. Collectively, these HIV-induced alterations of host defense explain the increased susceptibility of HIV-infected persons for oropharyngeal candidiasis, bacterial pneumonia, and Pneumocystis jiroveci pneumonia.