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The Immunocompromised Host

HIV Infection

Division of Pulmonary and Critical Care Medicine, University of Michigan Medical School; and Medical Service, Department of Veterans Affairs Medical Center, Ann Arbor, Michigan

Correspondence and requests for reprints should be addressed to James M. Beck, M.D., Pulmonary Medicine (111G), Veterans Affairs Medical Center, 2215 Fuller Road, Ann Arbor, MI 48105. E-mail: jamebeck{at}umich.edu

ABSTRACT

The variety of pulmonary infections encountered in HIV-infected individuals indicates that many components of the host defense network are impaired. In addition to depletion of CD4+ T cell numbers, HIV infection results in functional deficits in CD4+ T cells, CD8+ T cells, and natural killer cells. Although some components of macrophage defense are preserved, lack of activation signals from CD4+ T cells contributes to impaired defense by macrophages. There are few data examining the functional capabilities of neutrophils in the lung, but evidence from peripheral blood neutrophils indicates that defense by these cells is also impaired. An improved understanding of these events in the lung during HIV infection could lead to specific interventions aimed at restoration of deficient function.

Key Words: HIV infections • macrophages, alveolar • neutrophils • opportunistic infections • T-lymphocytes

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