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Virology. 2015 Oct;484:377-85. doi: 10.1016/j.virol.2015.06.010. Epub 2015 Jul 28.

Bovine herpesvirus 1 productive infection and immediate early transcription unit 1 promoter are stimulated by the synthetic corticosteroid dexamethasone.

Author information

1
School of Veterinary Medicine and Biomedical Sciences, Nebraska Center for Virology, University of Nebraska, Morisson Life Science Center, RM234, Lincoln, NE 68583-09065, USA.
2
Mississippi State University, Department of Biochemistry and Molecular Biology, Entomology and Plant Pathology, 408 Dorman Hall-Mailstop 9655, 32 Creelman St., Starkville, MS 39762, USA.
3
School of Veterinary Medicine and Biomedical Sciences, Nebraska Center for Virology, University of Nebraska, Morisson Life Science Center, RM234, Lincoln, NE 68583-09065, USA. Electronic address: clint.jones10@okstate.edu.

Abstract

The primary site for life-long latency of bovine herpesvirus 1 (BHV-1) is sensory neurons. The synthetic corticosteroid dexamethasone consistently induces reactivation from latency; however the mechanism by which corticosteroids mediate reactivation is unclear. In this study, we demonstrate for the first time that dexamethasone stimulates productive infection, in part, because the BHV-1 genome contains more than 100 potential glucocorticoid receptor (GR) response elements (GREs). Immediate early transcription unit 1 (IEtu1) promoter activity, but not IEtu2 or VP16 promoter activity, was stimulated by dexamethasone. Two near perfect consensus GREs located within the IEtu1 promoter were necessary for dexamethasone-mediated stimulation. Electrophoretic mobility shift assays and chromatin immunoprecipitation studies demonstrated that the GR interacts with IEtu1 promoter sequences containing the GREs. Although we hypothesize that DEX-mediated stimulation of IEtu1 promoter activity is important during productive infection and perhaps reactivation from latency, stress likely has pleiotropic effects on virus-infected cells.

KEYWORDS:

BHV-1; Glucocorticoid receptor; Glucocorticoid response element; Immediate early transcription unit 1; Stress-induced viral replication

PMID:
26226582
DOI:
10.1016/j.virol.2015.06.010
[Indexed for MEDLINE]
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