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The Journal of Immunology, 2000, 164: 4955-4960.
Copyright © 2000 by The American Association of Immunologists

Macrophage Colony-Stimulating Factor Antagonists Inhibit Replication of HIV-1 in Human Macrophages

Joseph Kutza1,*, Lynne Crim{dagger}, Steven Feldman{dagger}, Mark P. Hayes§, Marion Gruber{ddagger}, Judy Beeler{dagger} and Kathleen A. Clouse*

* Division of Monoclonal Antibodies, Office of Therapeutics Research and Review, and Divisions of {dagger} Viral Products and {ddagger} Vaccines and Related Products Applications, Office of Vaccines Research and Review, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD 20892; and § Genzyme Corp., Framingham, MA 01701

Macrophages infected with HIV-1 produce high levels of M-CSF and macrophage-inflammatory protein-1{alpha} (MIP-1{alpha}). M-CSF facilitates the growth and differentiation of macrophages, while the chemotactic properties of MIP-1{alpha} attract both T lymphocytes and macrophages to the site of HIV infection. Studies described in this work indicate M-CSF may function in an autocrine/paracrine manner to sustain HIV replication, and data suggest possible therapeutic strategies for decreasing viral load following HIV infection. We show that macrophage infection with measles virus or respiratory syncytial virus, in contrast to HIV-1, results in production of MIP-1{alpha}, but not M-CSF. Thus, M-CSF appears to be specifically produced upon infection of macrophages with HIV-1. Furthermore, addition of M-CSF antagonists to HIV-1-infected macrophages, including anti-M-CSF monoclonal or polyclonal Abs or soluble M-CSF receptors, dramatically inhibited HIV-1 replication and reduced production of MIP-1{alpha}. Our results suggest that biologic antagonists for M-CSF may represent novel strategies for inhibiting the spread of HIV-1 by 1) blocking virus replication in macrophages, 2) reducing recruitment of HIV-susceptible T cells and macrophages by MIP-1{alpha}, and 3) preventing the establishment and maintenance of infected macrophages as a reservoir for HIV.




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