Activation of transcription from the human immunodeficiency virus type 1 (HIV-1) long terminal repeat by the vasoactive intestinal peptide (VIP).
The ability of the human immunodeficiency virus type 1 (HIV-1) to persist and replicate in human CD4+ cells is under the control of both virally encoded proteins and a variety of host-related factors. Transcription of human immunodeficienty virus type 1 (HIV-1) is regulated by multiple cis-acting regulatory elements located in the viral long terminal repeats (LTRs). Here we report that the human vasoactive intestinal peptide (VIP) can activate the HIV-1-LTR. The activity of VIP is dose-dependent and specific. The effective concentration of VIP is within the physiological range suggesting that VIP release may modulate the activity of HIV-1 in vivo. A sequence in U3 region could be involved in VIP and in various VIP-related peptides' activation of HIV-1-LTR. This cis-acting element conferring VIP responsiveness is indistinguishable from HIV NF-kappa B tandem repeat binding sites (HIV-1 kappa B).
Gilles
A
A
Université de Provence, Marseille, France.
Miquelis
A
A
Luis
J
J
Faure
E
E
D004742:Enhancer Elements, Genetic; D016325:HIV Long Terminal Repeat; D015497:HIV-1 / Q000235:genetics*; D019073:HT29 Cells; D006801:Humans; D016328:NF-kappa B / Q000378:metabolism; D015533:Transcriptional Activation; D014162:Transfection; D014407:Tumor Cells, Cultured; D014660:Vasoactive Intestinal Peptide / Q000494:pharmacology*
D016328:NF-kappa B; D014660:Vasoactive Intestinal Peptide