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J Virol, July 1998, p. 6264-6270, Vol. 72, No. 7
Viral Pathogenesis Laboratory,
Received 29 July 1997/Accepted 17 April 1998
Expression of human T-cell leukemia virus type 1 (HTLV-1) is
regulated both by the HTLV-1 Tax transactivator and
by cellular transcriptional factors binding to the viral long terminal
repeat (LTR), suggesting that cellular signals may
play a role in regulating viral expression. Treatment of cells
chronically infected with HTLV-1, which express low levels of HTLV-1
RNAs and Tax protein, with phorbol esters (i.e., phorbol12-myristate
13- acetate [PMA]), phytohemagglutinin (PHA), sodium
butyrate, or combinations of cytokines resulted in induction of
HTLV- 1 gene expression. PMA or PHA treatment following
cotransfection of HTLV-1 Tax expression plasmids resulted
in synergistic activation of HTLV-1 LTR-directed gene expression,
apparently involving tyrosine ki- nase- mediated pathways. These results suggest that cellular activation stimuli may
cooperate with HTLV-1 Tax to enhance expression of integrated HTLV-1 genomes and thus may play a role in the pathogenesis of HTLV-1
disease.
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Activation of Human T-Cell Leukemia Virus Type 1 tax Gene Expression in Chronically Infected T
Cells
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Corresponding author. Mailing address: CABM, Rm. 139, 679 Hoes Ln., Piscataway, NJ 08854. Phone: (908) 235-5368. Fax: (908) 235-4850. E-mail: rabson{at}mbcl.rutgers.edu.
J Virol, July 1998, p. 6264-6270, Vol. 72, No. 7
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
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