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Division of Monoclonal Antibodies, Office of Therapeutics Research and Review, and Divisions of
Viral Products and
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
(MIP-1). M-CSF facilitates the
growth and differentiation of macrophages, while the chemotactic
properties of MIP-1 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, 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. 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, and 3) preventing the establishment and
maintenance of infected macrophages as a reservoir for
HIV.
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