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Inhibition of CXCR4-Tropic HIV-1 Infection by Lipopolysaccharide: Evidence of Different Mechanisms in Macrophages and T Lymphocytes¹

Alessia Verani^2,*, Francesca Sironi^*, Antonio G. Siccardi, Paolo Lusso^* and Donata Vercelli

^* Human Virology Unit, DIBIT, San Raffaele Scientific Institute, and Department of Biology and Genetics, University of Milan, Milan, Italy; and Respiratory Sciences Center, College of Medicine, University of Arizona, Tucson, AZ 85724

Bacterial LPS protects primary human macrophages from infection by CCR5-tropic HIV-1 isolates through the release of the CC chemokines RANTES and macrophage inflammatory protein-1 and -1. Here, we show that LPS also suppresses infection of macrophages by CXCR4-tropic HIV-1 isolates. A marked down-regulation of both CD4 and CXCR4 expression was associated with this effect. Furthermore, a soluble factor(s) released by macrophages upon LPS treatment inhibited infection with CXCR4-tropic HIV-1 isolate viruses in both macrophages and T lymphocytes. Infection of both cell types appeared to be blocked at the level of viral entry and was independent of stromal cell-derived factor-1, the only known natural ligand of CXCR4. Moreover, the suppressive effect of LPS was unrelated to the release of IFN- and -, macrophage-derived chemokine, leukemia inhibitory factor, or TNF-. These results suggest the existence of potent HIV-1 inhibitory factor(s), uncharacterized to date, released by activated cells of the mononuclear phagocytic system.

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