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J Gen Virol 69 (1988), 2913-2917; DOI 10.1099/0022-1317-69-11-2913
© 1988 Society for General Microbiology

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Heat-shock Induction of the Human Immunodeficiency Virus Long Terminal Repeat

J. L. M. C. Geelen1, R. P. Minnaar1, R. Boom1, J. Van Der Noordaa1 and J. Goudsmit2

1 Department of Virology, Academic Medical Center, University of Amsterdam, Meibergdreef 15
and2 Human Retrovirus Laboratory, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands

Rat cell lines were established in which the bacterial chloramphenicol acetyltransferase (CAT) gene under control of the human immunodeficiency virus (HIV) long terminal repeat (LTR) was stably integrated. The cell lines showed a repressed phenotype for CAT expression, but could be induced for it by inhibition of protein synthesis, as well as by heat-shock and chemical inducers of the cellular stress response, such as sodium arsenite, 8-hydroxyquinoline and the heavy metals cadmium and copper. A decameric sequence present in the NF-kB binding sites in the HIV LTR (GGGACTTTCC) resembles the cellular heat-shock core sequence and may therefore be involved in the heat-shock response.

Keywords: HIV, heat-shock, LTR

Received 8 December 1987; accepted 25 July 1988.


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