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Am. J. Respir. Crit. Care Med., Volume 162, Number 3, September 2000, 966-970

Human Immunodeficiency Virus Type 1 Infection of Alveolar Macrophages Impairs Their Innate Fungicidal Activity

MICHAEL H. IEONG, CHRISTINE CAMPBELL REARDON, STUART M. LEVITZ, and HARDY KORNFELD

Pulmonary Center, Evans Memorial Department of Clinical Research, and the Department of Medicine, Boston University School of Medicine, Boston, Massachusetts

Impaired adaptive immunity is the hallmark of AIDS, but the effects of human immunodeficiency virus type 1 (HIV-1) infection on innate immunity are less clear. Cryptococcus neoformans (CN) is a common AIDS-related fungal pathogen acquired by inhalation. Alveolar macrophages (AMphi) comprise the initial host defense in cryptococcosis and they may arrest infection before dissemination occurs. We hypothesized that HIV-1 infection of AMphi impairs their anti-cryptococcal activity. This was tested by infection of normal AMphi with the M-tropic strain HIV-1Bal. Two weeks postinfection we measured fungistatic activity against CN by colony counting, binding, and internalization of CN by confocal microscopy and AMphi cell viability by Alamar Blue assay. Uninfected AMphi from most donors demonstrated innate fungicidal activity against CN. In HIV-1-infected AMphi, there was a significant reduction, and in most cases loss, of fungicidal activity compared with the uninfected AMphi. The reduced antifungal activity was not due to any cytotoxic effect of HIV-1, and HIV-1 infection did not impair binding or internalization of yeast by AMphi. Thus, the innate fungicidal activity of primary human AMphi is impaired after HIV-1 infection in vitro by a mechanism involving a defect of intracellular antimicrobial processing.




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