Premium
Examination of TAR‐independent trans activation by human immunodeficiency virus type 1 Tat in human glial cells
Author(s) -
Kim Y.S.,
Panganiban A.T.
Publication year - 1996
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19960315)43:6<652::aid-jnr2>3.0.co;2-d
Subject(s) - biology , long terminal repeat , hiv long terminal repeat , heterologous , reporter gene , transfection , tar (computing) , microbiology and biotechnology , gene , cell culture , gene expression , heterologous expression , virology , recombinant dna , genetics , computer science , programming language
Astrocytic glial cells derived from central nervous system (CNS) can support human immunodeficiency virus type 1 (HIV‐1) replication in cell culture, may be infected in tissue culture, and are thought to be a large HIV‐1 reservoir in vivo. The Tat protein of HIV‐1 interacts with a cis ‐acting target sequence referred to as TAR. However, Tat can also stimulate gene expression directed from some heterologous promoters and, in certain circumstances, an HIV‐1 long terminal repeat (LTR) that lacks the TAR element. Therefore, we attempted to investigate Tat trans activation of HIV‐1 LTR in the astrocytic glial cells. Using transfection of LTR‐reporter gene constructs and HIV‐1 proviral constructs, we demonstrate TAR‐dependent replication in astrocytic cells. We also examined the expression of HIV‐1 env gene from an LTR that lacks TAR element. In a previous study (Kim and Panganiban: J Virol 67:3739–3747, 1993), we observed that env expression is trans activated only by the full‐length Tat protein through a TAR‐independent manner in HeLa cells. However, in astrocytic glial cells, the trans activation of env expression from the LTR‐lacking TAR element was mediated by the first exon peptide of Tat as well as the full‐length Tat peptide through a post‐transcriptional mechanism rather than a transcriptional one. This result suggests that cell type‐specific factor(s) is involved in the TAR‐independent Tat responsiveness. © 1996 Wiley‐Liss, Inc.