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Sequences from 420 to 70 from the ICP0 transcriptional start site of herpes simplex virus type 1 are dispensable for reactivation from latency. A putative cAMP-response element (CRE) outside of this region was non-functional in both murine neuroblastoma (NB41A3) and rat pheochromo- cytoma (PC12) cells. Also, poor binding of cAMP- response element binding protein (CREB) was observed. Sequences from 95 to 37 are important for constitutive activity in NB41A3, PC12 and baby hamster kidney (BHK) cells. The TATA box and Sp1 site were also shown to be major contributors to constitutive activity. Finally, high constitutive activity of a deleted construct (N420 to 1) in NB41A3 and BHK cells suggests transcription initiates upstream of 420 in the absence of VP16. The implications of these observations regarding ICP0 expression during the virus life-cycle are discussed.
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