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Upstream stimulating factor affects human immunodeficiency virus type 1 (HIV-1) long terminal repeat-directed transcription in a cell-specific manner, independently of the HIV-1 subtype and the core-negative regulatory element

Division of Clinical Virology, Karolinska Institute, F68, Huddinge University Hospital, S-141 86 Huddinge, Stockholm, Sweden¹
Department of Medical Biochemistry and Microbiology, BMC, Uppsala University, S-751 23 Uppsala, Sweden²
Laboratory of Biochemistry and Molecular Biology, The Rockefeller University, 1230 York Avenue, New York 10021-6399, USA³

Author for correspondence: Mojgan H. Naghavi. Fax +46 8 585 87933. e-mail Mojgan.Naghavi{at}impi.ki.se

Human immunodeficiency virus type 1 (HIV-1) is classified into subtypes on the basis of phylogenetic analysis of sequence differences. Inter- and intra-subtype polymorphism extends throughout the genome, including the long terminal repeat (LTR). In this study, the importance of the upstream stimulating factor (USF)-binding site (E-box) in the core-negative regulatory element (NRE) of the LTR of HIV-1 subtypes A, B, C, D, E and G was investigated. In vivo, USF was found to repress transcription directed from representative HIV-1 LTR sequences of all the subtypes tested in an epithelial cell line, yet activate the same transcription in a T-cell line. Mutation of the core-NRE USF site of the representative subtype B LTR did not affect the cell-specific, subtype-independent, dual role of USF. In vitro binding assays showed that recombinant USF⁴³ interacts with the core-NRE from subtypes B and C, but not A, D, E or G. Thus, USF affects LTR-directed transcription in a cell-specific manner, independently of both the HIV-1 subtype from which the LTR was derived and the core-NRE USF site sequences.

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