The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1997/3/805/ $5.00
The Journal of Experimental Medicine, Volume 185, Number 5, March 3, 1997 805-816

Articles

C–C Chemokines Released by Lipopolysaccharide (LPS)-stimulated Human Macrophages Suppress HIV-1 Infection in Both Macrophages and T Cells

Alessia Verani*, Gabriella Scarlatti{ddagger}, Manola Comar||, Eleonora Tresoldi{ddagger}, Simona Polo§, Mauro Giacca||, Paolo Lusso§, Antonio G. Siccardi{ddagger},¶, and Donata Vercelli*

From the * Molecular Immunoregulation, {ddagger} Lymphocyte Differentiation, and § Human Virology Unit, Department of Biological and Technological Research, San Raffaele Scientific Institute, 20132 Milan, || International Center for Genetic Engineering and Biotechnology, 34012 Trieste, and Department of Biology and Genetics, University of Milan, 20100 Milan, Italy

Human immunodeficiency virus-1 (HIV-1) expression in monocyte-derived macrophages (MDM) infected in vitro is known to be inhibited by lipopolysaccharide (LPS). However, the mechanisms are incompletely understood. We show here that HIV-1 suppression is mediated by soluble factors released by MDM stimulated with physiologically significant concentrations of LPS. LPS-conditioned supernatants from MDM inhibited HIV-1 replication in both MDM and T cells. Depletion of C–C chemokines (RANTES, MIP-1{alpha}, and MIP-1β) neutralized the ability of LPS-conditioned supernatants to inhibit HIV-1 replication in MDM. A combination of recombinant C–C chemokines blocked HIV-1 infection as effectively as LPS. Here, we report an inhibitory effect of C–C chemokines on HIV replication in primary macrophages. Our results raise the possibility that monocytes may play a dual role in HIV infection: while representing a reservoir for the virus, they may contribute to the containment of the infection by releasing factors that suppress HIV replication not only in monocytes but also in T lymphocytes.

Address correspondence to Donata Vercelli, MD, Molecular Immunoregulation Unit, DIBIT, San Raffaele Scientific Institute, Via Olgettina 58, 20132 Milano, Italy.

1Abbreviations used in this paper: MDM, monocyte-derived macrophages; MIP, macrophage inflammatory protein; NSI, nonsyncitium-inducing; RANTES, regulated upon activation, normal T expressed and secreted; RT, reverse transcriptase.


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