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 immunodeficiency 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 the 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 kB).