from Part II - Basic virology and viral gene effects on host cell functions: alphaherpesviruses
Published online by Cambridge University Press: 24 December 2009
The regulated transcription of the HSV IE (immediate–early, α) genes has been a model system for elucidating principles and mechanisms of combinatorial-differential regulation, basic RNAPII -directed transcription, and multiprotein assembly specificities. The regulation exemplifies viral mechanisms dedicated to the recruitment of cellular components into complex viral–host interactions that illustrate general parameters of protein–protein, DNA –protein, RNA transcription, and protein complex assembly. Continued studies hold promise of advancing the understanding of the complexities of biochemical interactions in gene expression as well as complex cellular response pathways. The regulation of the IE genes within specific contexts may also lead to the understanding of signals and pathways which modulate viral infection and determine the extent of lytic-latent infection. While HSV has been extensively studied and will represent the focus of this review, the regulatory domain of the VZV IE gene (IE62) contains similar elements and is regulated by similar mechanisms.
The HSV IE regulatory domains: multiple sites for differential regulation
The regulatory domains of the HSV IE genes have been the focus of numerous studies that have defined the sequence elements and their contributions to the basal and induced levels of transcription. These IE domains typically consist of a reiterated inducible enhancer core element (consensus: TAATGARAT) that is flanked by binding sites for members of the ets and kruppel transcription family (Fig. 8.1, left) (Roizman and Sears, 1996; Vogel and Kristie, 2001).
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