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J Biol Chem, Vol. 273, Issue 42, 27306-27314, October 16, 1998

Prostaglandin E₂ Up-regulates HIV-1 Long Terminal Repeat-driven Gene Activity in T Cells via NF-B-dependent and -Independent Signaling Pathways

From the Centre de Recherche en Infectiologie, Centre Hospitalier Universitaire de Québec, Pavillon CHUL, and Département de Biologie médicale, Faculté de Médecine, Université Laval, Ste-Foy, Québec G1V 4G2, Canada

Replication of human immunodeficiency virus type-1 (HIV-1) is highly dependent on the state of activation of the infected cells and is modulated by interactions between viral and host cellular factors. Prostaglandin E₂ (PGE₂), a pleiotropic immunomodulatory molecule, is observed at elevated levels during HIV-1 infection as well as during the course of other pathogenic infections. In 1G5, a Jurkat-derived T cell line stably transfected with a luciferase gene driven by HIV-1 long terminal repeat (LTR), we found that PGE₂ markedly enhanced HIV-1 LTR-mediated reporter gene activity. Experiments have been conducted to identify second messengers involved in this PGE₂-dependent up-regulating effect on the regulatory element of HIV-1. In this study, we present evidence indicating that signal transduction pathways induced by PGE₂ necessitate the participation of cyclic AMP, protein kinase A, and Ca²⁺. Experiments conducted with different HIV-1 LTR-based vectors suggested that PGE₂-mediated activation effect on HIV-1 transcription was transduced via both NF-B-dependent and -independent signaling pathways. The involvement of NF-B in the PGE₂-dependent activating effect on HIV-1 transcription was further confirmed using a B-regulated luciferase encoding vector and by electrophoretic mobility shift assays. Results from Northern blot and flow cytometric analyses, as well as the use of a selective antagonist indicated that PGE₂ modulation of HIV-1 LTR-driven reporter gene activity in studied T lymphoid cells is transduced via the EP₄ receptor subtype. These results suggest that secretion of PGE₂ by macrophages in response to infection or inflammatory activators could induce signaling events resulting in activation of proviral DNA present into T cells latently infected with HIV-1.

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