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Trans-activation of Long Terminal Repeat Sequence-mediated Gene Expression Is Not a Property of Type D Retrovirus Replication

¹ Departments of Medicine, and Microbiology and Immunology, Washington University, St. Louis, Missouri 63110
² Department of Microbiology, University of Alabama, Birmingham, Alabama 35294
and³ Department of Microbiology, New England Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772, U.S.A.

Several retroviruses encode trans-acting factors which activate gene expression directed by long terminal repeat (LTR) sequences and play a role in the positive feedback regulation of virus replication. We have examined two Mason-Pfizer monkey virus (MPMV) strains for their ability to produce and respond to such factors. Plasmids with the LTR of either MPMV or type D retrovirus/New England (D/NE) were fused to the bacterial chloramphenicol acetyltransferase (CAT) gene. Introduction of these plasmids into several different human cell lines gave rise to significant CAT activity, demonstrating the strong transcriptional promoter activity of these LTRs. However, little or no increase in CAT activity was found upon transfection of these plasmids into MPMV- or D/NE-infected cell lines as compared with uninfected cell lines. Furthermore, CAT activity was not enhanced in uninfected cells by cotransfecting either a functional MPMV DNA clone, a plasmid expressing the human T-lymphotropic retrovirus trans-activator genes, tat-1 or tat-3. These data show that the property of trans-activation of LTR-mediated gene expression is a function in the replication of only certain retroviruses.

Keywords: trans-activation, long terminal repeats, retroviruses, type D

Received 2 March 1987; accepted 13 May 1987.

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