期刊
VIROLOGY
卷 505, 期 -, 页码 71-79出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2017.02.012
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资金
- USDA-NIFA Competitive Grants Program [13-01041, 16-09370]
- Sitlington Endowment
- Oklahoma Center for Respiratory and Infectious Diseases (National Institutes of Health Centers for Biomedical Research) [P20GM103648]
- China Scholarship Council
- Chinese National Science Foundation [31472172]
- National Key Research Program [2016YFD0500704]
- National Institute for General Medical Science (NIGMS) [INBRE-P20GM103427-14, COBRE 1P30GM110768-01]
- Fred & Pamela Buffett Cancer Center [P30CA036727]
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.
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