Abstract
In the past five years since their discovery, enhancer elements have been studied intensively in a large number of laboratories (see refs. 1,2). The prototype enhancer element, the 72-bp repeat of SV40, was first shown to be an essential set of sequences required for the efficient transcription of SV40 early genes [3–5]. Although there is some variability in the sequences that we have come to know as enhancers, in general their definition involves the following common properties: They are short sets of nucleotides (50–100 bp in length), often repeated in tandem, which work in concert with the other promoter elements to increase the efficiency of transcription of an associated gene as much as 100–1000 fold. A remarkable feature of enhancer elements is their relative position- and orientation-independence. For example, the SV40 72-bp repeat element will activate transcription from a promoter when located in either orientation, 5′ or 3′ to the cap site, and several kilobases away. Enhancer elements can generally act on heterologous genes as well as on the natural promoter with which they are associated [6,7]. Finally, a number of enhancer elements show tissue or species specificity, which contributes significantly to the host range of the virus with which they are associated [8–10]. In this review, we discuss the possibility that enhancer specificity not only contributes to the target tissue in which the virus is active, but also frequently dictates the disease potential of the viral agent.
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Brady, J., Feigenbaum, L., Khoury, G. (1986). Viral Enhancer Elements. In: Notkins, A.L., Oldstone, M.B.A. (eds) Concepts in Viral Pathogenesis II. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-4958-0_8
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DOI: https://doi.org/10.1007/978-1-4612-4958-0_8
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