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Upstream Stimulatory Factor Family Binds to the Herpes Simplex Virus Type 1 Latency-Associated Transcript Promoter
Journal article   Open access   Peer reviewed

Upstream Stimulatory Factor Family Binds to the Herpes Simplex Virus Type 1 Latency-Associated Transcript Promoter

Joseph J Kenny, Scott Millhouse, Michael Wotring and Brian Wigdahl
Virology (New York, N.Y.), v 230(2), pp 381-391
14 Apr 1997
PMID: 9143295
url
https://doi.org/10.1006/viro.1997.8501View
Published, Version of Record (VoR) Open

Abstract

The herpes simplex virus type 1 (HSV-1) latency-associated transcript (LAT) promoter 1 (LP1) is the only viral promoter that exhibits detectable transcriptional activity during a latent HSV infection. The LAT promoter-binding factor (LPBF) regulatory sequence (nucleotides −65 to −72 relative to the transcriptional start site of the 8.3-kb primary transcript) closely resembles the core recognition sequence required for binding members of the upstream stimulatory factor (USF)/major late transcription factor (MLTF) family. In this analysis, we demonstrate that oligonucleotides containing either the LPBF recognition sequence or the USF/MLTF recognition sequences from previously described promoters bind cellular factors which exhibit very similar mobilities in electrophoretic mobility shift (EMS) analyses. We also observe a high degree of similarity in competition profiles obtained in competition EMS analyses utilizing oligonucleotides containing recognition sequences for either LPBF or USF/MLTF. Furthermore, antibody supershift EMS analyses have demonstrated that the factors binding the LPBF or USF/MLTF recognition sites in these oligonucleotides are antigenically related, if not identical, and that greater than 90% of the LPBF-binding activity is antigenically related to USF. In addition, we demonstrate that both forms ofin vitro-translated USF proteins (43 and 44 kDa) bind to the LPBF recognition sequence within HSV-1 LP1. Taken together, these data indicate that USF is capable of binding to the HSV-1 LPBF recognition sequence and that USF is a major LPBF-binding activity in cells of neuronal and nonneuronal lineage. These data further support the hypothesis that USF may indeed play a significant role in the transcriptional activity of HSV-1 LP1.

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