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Updated: Aug 19, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
The herpesvirus saimiri Rta gene autostimulates via binding to a non-consensus response element
Matthew S Walters1, Kersten T Hall2, Adrian Whitehouse3,1
1School of Biochemistry and Microbiology, University of Leeds, Leeds LS2 9JT, UK.
Abstract:
Herpesvirus saimiri ORF 50a protein expression is sufficient to reactivate the entire lytic-replication cycle. ORF 50a functions as a sequence-specific transactivator that is capable of activating delayed-early gene expression via direct binding to an ORF 50 response element (RE) within the respective promoter. Here, it is shown that ORF 50a is capable of transactivating its own promoter. Deletion analysis of the ORF 50a promoter showed that the ORF 50-responsive element is contained within an 80 bp fragment, situated 293-373 bp from the transcription initiation site. Gel-retardation analysis further mapped the RE to a 34 bp fragment that was able to confer ORF 50 responsiveness to an enhancerless SV40 minimal promoter. Sequence analysis showed that this RE has no direct similarity to previously identified ORF 50 REs. Therefore, it is concluded that ORF 50a is capable of stimulating its own promoter via a novel RE.
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