title: Effects of the synthetic corticosteroid dexamethasone on bovine herpesvirus 1 productive infection.
abstract: Sensory neurons are a primary site for life-long latency of bovine herpesvirus 1 (BoHV-1). The synthetic corticosteroid dexamethasone induces reactivation from latency and productive infection, in part because the BoHV-1 genome contains more than 100 glucocorticoid receptor (GR) responsive elements (GREs). Two GREs in the immediate early transcription unit 1 promoter are required for dexamethasone induction. Recent studies also demonstrated that the serum and glucocorticoid receptor protein kinase (SGK) family stimulated BoHV-1 replication. Consequently, we hypothesized that dexamethasone influences several aspects of productive infection. In this study, we demonstrated that dexamethasone increased expression of the immediate early protein bICP4, certain late transcripts, and UL23 (thymidine kinase) by four hours after infection. SGK1 expression and Akt phosphorylation were also stimulated during early stages of infection and dexamethasone treatment further increased this effect. These studies suggest that stress, as mimicked by dexamethasone treatment, has the potential to stimulate productive infection by multiple pathways.
authors.affiliation: Oklahoma State University, Center for Veterinary Health Sciences, Department of Veterinary Pathobiology, Stillwater, OK 74078, USA; College of Veterinary Medicine and Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, 48 Wenhui East Road, Yangzhou 225009, China.
authors.forename: Liqian
authors.initials: L
authors.lastname: Zhu
authors.affiliation: University of Nebraska, Nebraska Center for Virology, Morisson Life Science Center, Lincoln, NE 68583-09065, USA.
authors.forename: Jesse
authors.initials: J
authors.lastname: Thompson
authors.affiliation: University of Nebraska, Nebraska Center for Virology, Morisson Life Science Center, Lincoln, NE 68583-09065, USA.
authors.forename: Fangrui
authors.initials: F
authors.lastname: Ma
authors.affiliation: Department of Genetics Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, Nebraska, USA.
authors.forename: James
authors.initials: J
authors.lastname: Eudy
authors.affiliation: Oklahoma State University, Center for Veterinary Health Sciences, Department of Veterinary Pathobiology, Stillwater, OK 74078, USA.
authors.forename: Clinton
authors.initials: C
authors.lastname: Jones
mesh_terms: D000818:Animals; D002417:Cattle; D002478:Cells, Cultured; D003907:Dexamethasone / Q000494:pharmacology*; D005938:Glucocorticoids / Q000494:pharmacology*; D006566:Herpesviridae Infections / Q000139:chemically induced*; D007242:Herpesvirus 1, Bovine / Q000187:drug effects*; D010766:Phosphorylation; D011401:Promoter Regions, Genetic; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism*; D011965:Receptors, Glucocorticoid / Q000235:genetics; D014759:Viral Envelope Proteins / Q000096:biosynthesis*; D014775:Virus Activation / Q000187:drug effects*; D017735:Virus Latency / Q000502:physiology
chemical_list: D005938:Glucocorticoids; D011965:Receptors, Glucocorticoid; D014759:Viral Envelope Proteins; C083786:immediate early protein BICP4, bovine herpesvirus 1; D003907:Dexamethasone; D020794:Receptor Protein-Tyrosine Kinases; D051057:Proto-Oncogene Proteins c-akt