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The Journal of Immunology, 1998, 160: 2881-2888.
Copyright © 1998 by The American Association of Immunologists

The Lipophosphoglycan of Leishmania donovani Up-Regulates HIV-1 Transcription in T Cells Through the Nuclear Factor-{kappa}B Elements1

Richard Bernier, Benoît Barbeau, Michel J. Tremblay2 and Martin Olivier2

Centre de Recherche en Infectiologie, Centre Hospitalier Universitaire de Québec, Pavillon du Centre Hospitalier de l’Université Laval (CHUL), and Département de Biologie Médicale, Faculté de Médecine, Université Laval, Ste-Foy, Québec, Canada

We have recently demonstrated that the parasite Leishmania donovani and its surface molecule, lipophosphoglycan (LPG), can activate HIV-1 replication in monocytoid cells. Our present interest was to determine whether LPG could also up-regulate HIV-1 transcription in T cells. Using a CD4-positive human lymphoid T cell line (1G5) containing a stably integrated HIV-1 long terminal repeat (LTR)-luciferase construct, we found that LPG is a potent inducer of HIV-1 LTR activity. Treatment of 1G5 cells with signaling antagonists revealed that protein tyrosine kinase- and protein kinase A-dependent pathways were actively participating in the LPG-induced enhancement of HIV-1 LTR-driven activity. Transfection of Jurkat E6.1 cells with plasmids containing wild-type and nuclear factor-{kappa}B (NF-{kappa}B)-mutated HIV-1 LTR-luciferase constructs has suggested a role for NF-{kappa}B binding sites in the LPG-mediated induction of HIV-1 LTR activity. An LPG-induced binding factor specific to the NF-{kappa}B consensus sequences could be observed using electrophoretic mobility shift assay. Finally, transfection experiments performed with a vector containing HIV-1 {kappa}B binding sites only showed similar LPG-mediated induction, which was abrogated by sodium salicylate, a known NF-{kappa}B inhibitor. We thus demonstrate that the LPG-mediated induction of HIV-1 LTR activity in T cells involves several second messengers culminating in activation of HIV-1 LTR-driven transcription via NF-{kappa}B-binding consensus sequences. In conclusion, these results reinforce the idea that L. donovani is a putative cofactor in HIV-1 pathogenesis.




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