YY1 is the cellular factor shown previously to bind to regulatory regions of several leaky-late (beta gamma, gamma 1) genes of herpes simplex virus type 1.

We have recently reported that a cellular factor, the leaky-late binding factor (LBF), binds to sites in a number of leaky-late (beta gamma or gamma 1) genes of herpes simplex virus type 1 and that an LBF site is essential for maximum viral transactivation of the major capsid protein (VP5) gene. The results of binding competition, partial proteolysis, and monoclonal antibody inhibition assays presented here establish that LBF is identical to the transcription factor YY1. This, along with our previous observations, suggests that YY1 plays a role in herpes simplex virus type 1 gene regulation.

Transactivation of the major capsid protein gene of herpes simplex virus type 1 requires a cellular transcription factor.

The purpose of this investigation was to identify and characterize the regulatory elements involved in the transcriptional activation of the beta gamma (leaky-late or gamma 1) genes of herpes simplex virus type 1 (HSV-1) by using the major capsid protein (VP5 or ICP5) gene as model. Gel mobility shift assays with nuclear extracts from uninfected and infected HeLa cells enabled us to identify two major protein-DNA complexes involving the VP5 promoter. The mobilities of these two complexes remained unaltered, and no unique complexes were observed when infected cell nuclear extracts were used.

In vitro transcription of herpes simplex virus genes: identification of a new initiation site and second intervening sequence in the immediate-early RNA-5 gene.

We have used partially purified preparations of RNA polymerase II from mock-infected and herpes simplex virus type 1-infected HEp-2 cells to transcribe the herpes simplex virus type 1 strain F BamHI Z DNA fragment containing the promoter for immediate-early RNA-5 (alpha 47), a 1.8-kilobase, spliced RNA. In agreement with the in vivo transcriptional regulation of herpes simplex virus type 1 immediate-early genes, electrophoretic analyses of runoff and truncated transcripts from this template showed that RNA polymerase II from mock-infected cells initiates transcription more selectively than does that from the herpes virus-infected cells at the immediate-early RNA-5 promoter.