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

Insun Kook, Caitlin Henley, Florencia Meyer, Federico G. Hoffmann, Clinton Jones

Research output: Contribution to journalArticle

22 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)377-385
Number of pages9
JournalVirology
Volume484
DOIs
StatePublished - Oct 1 2015
Externally publishedYes

Keywords

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

ASJC Scopus subject areas

  • Virology

Fingerprint Dive into the research topics of 'Bovine herpesvirus 1 productive infection and immediate early transcription unit 1 promoter are stimulated by the synthetic corticosteroid dexamethasone'. Together they form a unique fingerprint.

  • Cite this