The lipophosphoglycan of Leishmania donovani up-regulates HIV-1 transcription in T cells through the nuclear factor-kappaB elements.

摘要: 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 transcription T Using a CD4-positive human lymphoid cell line (1G5) containing stably integrated long terminal repeat (LTR)-luciferase construct, we found is potent inducer of LTR activity. Treatment 1G5 cells with signaling antagonists revealed protein tyrosine kinase- kinase A-dependent pathways were actively participating LPG-induced enhancement LTR-driven Transfection Jurkat E6.1 plasmids wild-type nuclear factor-kappaB (NF-kappaB)-mutated LTR-luciferase constructs has suggested role for NF-kappaB binding sites LPG-mediated induction An factor specific consensus sequences be observed using electrophoretic mobility shift assay. Finally, transfection experiments performed vector kappaB only showed similar induction, which abrogated by sodium salicylate, known inhibitor. thus demonstrate activity involves several second messengers culminating activation via NF-kappaB-binding sequences. In conclusion, these results reinforce idea L. putative cofactor pathogenesis.