Phagocytic Function of Monocyte-Derived Macrophages Is Not Affected by Human Immunodeficiency Virus Type 1 Infection

• Published in: The Journal of infectious diseases Vol. 168; no. 1; pp. 84 - 91
• Main Authors: Nottet, Hans S. L. M., de Graaf, Loek, de Vos, N. Machiel, Bakker, Leendert J., van Strijp, Jos A. G., Visser, Maarten R., Verhoef, Jan
• Format: Journal Article
• Language: English
• Published: Chicago, IL The University of Chicago Press 01.07.1993; University of Chicago Press
• Subjects: AIDS/HIV; Antigens, Surface - biosynthesis; Bacteria; Bacteriophages; Biological and medical sciences; Candida albicans - immunology; Cells, Cultured; Escherichia coli - immunology; Giant cells; HIV; HIV 1; HIV Infections - immunology; HIV-1 - physiology; human immunodeficiency virus; Immunodeficiencies; Immunodeficiencies. Immunoglobulinopathies; Immunopathology; Infections; Kinetics; Macrophages; Macrophages - cytology; Macrophages - immunology; Macrophages - microbiology; Major Articles; Medical sciences; Monoclonal antibodies; Monocytes - cytology; Monocytes - microbiology; Phagocytes; Phagocytosis; Polymerase Chain Reaction; Superoxides - metabolism; Viruses; Human; Immunopathology; Cell function; Pathophysiology; AIDS; Hemopathy; Cellular immunity; Bactericidal effect; Infection; Immunological investigation; Viral disease; Phagocytosis; Macrophage
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1093/infdis/168.1.84

The immunopathogenesis of human immunodeficiency virus (HIV) infection is characterized by the failure to control opportunistic infections. Here, the direct effect of HIV on macrophage phagocytic function was studied. HIV-1-infected monocyte-derived macrophages expressed as many Fe-r and complement receptors as did control macrophages. The function of these receptors was not affected by HIV-1 infection since binding and internalization of opsonized Escherichia coli and Staphylococcus aureus were not impaired. Production of reactive oxygen species induced by stimulation of the HIV-1-infected macrophages with opsonized E. coli, zymosan, or PMA was intact. HIV-I-infected macrophages killed opsonized E. coli and Candida albicans as effectively as did control macrophages. These results, therefore, do not support the hypothesis that HIV-1 infection of macrophages causes phagocytic dysfunction and suggest that HIV-induced abnormalities outside the mononuclear phagocyte system may lead to the inability to control opportunistic pathogens.