학술논문

Cell-to-cell contact activates the long terminal repeat of human immunodeficiency virus 1 through its ΚB motif.
Document Type
Article
Source
European Journal of Biochemistry. 3/1/97, Vol. 244 Issue 2, p568-574. 7p.
Subject
*IMMUNODEFICIENCY
*VIRUSES
*ENZYME activation
*PROTEINS
*FERTILIZATION in vitro
*IMMUNITY
Language
ISSN
0014-2956
Abstract
Cell-to-cell contact between peripheral blood lymphocytes and transfected human colonic carcinoma cell line HT29 activates transcription of the long terminal repeats (LTR) of human immunodeficiency virus. HIV-1 LTR transcription is controlled by a complex array of virus-encoded and cellular proteins. Using various constructs expressing a lacZ reporter gene under the control of the intact or three deleted forms of HIV-1 LTR, we obtained evidence that the κB regulatory elements located in the U3 region are involved in cell-to-cell activation of HIV-1 LTR. Cell-to-cell contact activates in vitro binding of the nuclear factor κB (NF-κB) p50/p65 heterodimer to an HIV-1 κB oligonucleotide. Cell-to-cell conflict activation of NF-κB was only partially inhibited by 100 μM pyrrolidine dithiocarbamate and was not correlated with a significant decrease of cellular inhibitor κBa. NF-κB nuclear activation was not detectable before 1 h after cell contact and was dependent on protein synthesis. [ABSTRACT FROM AUTHOR]