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Inhibits HIV-1 Replication in Peripheral Blood Monocytes and Alveolar Macrophages by Inducing the Production of RANTES and Decreasing C-C Chemokine Receptor 5 (CCR5) Expression1
Department of Internal Medicine, Divisions of
*
Infectious Diseases and
Pulmonary and Critical Care Medicine,
Graduate Program in Cellular and Molecular Biology, and
§
School of Public Health, University of Michigan Medical Center, Ann Arbor, MI 48109
The pathogenesis of HIV-1 infection is influenced by the
immunoregulatory responses of the host. Macrophages present in the
lymphoid tissue are susceptible to infection with HIV-1, but are
relatively resistant to its cytopathic effects and serve as a reservoir
for the virus during the course of disease. Previous investigators have
demonstrated that increased serum levels of TNF-
contribute to the
clinical symptoms of AIDS and that TNF- stimulates the production of
HIV-1 in chronically infected lymphocytic and monocytic cell lines by
increasing HIV-1 gene expression. Although previous studies have
suggested that TNF- may increase HIV-1 infection of primary human
mononuclear cells, some recent studies have indicated that TNF-
suppresses HIV-1 infection of macrophages. We now demonstrate that
TNF- suppresses HIV-1 replication in freshly infected peripheral
blood monocytes (PBM) and alveolar macrophages (AM) in a dose-dependent
manner. As TNF- has been shown to increase the production of C-C
chemokine receptor (CCR5)-binding chemokines under certain
circumstances, we hypothesized that TNF- inhibits HIV-1 replication
by increasing the expression of these HIV-suppressive factors. We now
show that TNF- treatment of PBM and AM increases the production of
the C-C chemokine, RANTES. Immunodepletion of RANTES alone or in
combination with macrophage inflammatory protein-1 and -1ß block
the ability of TNF- to suppress viral replication in PBM and AM. In
addition, we found that TNF- treatment reduces CCR5 expression on
PBM and AM. These findings suggest that TNF- plays a significant
role in inhibiting monocytotropic strains of HIV-1 by two distinct, but
complementary, mechanisms.
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