Cellular Transcription Factors Induced in Trigeminal Ganglia during Dexamethasone-Induced Reactivation from Latency Stimulate Bovine Herpesvirus 1 Productive Infection and Certain Viral Promoters
Autor: | Aspen M. Workman, Devis Sinani, Clinton Jones, Halie Bricker, Emily Cook, Alan R. Doster, Leticia Frizzo da Silva, James D. Eudy, Lynette M. Smith |
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Rok vydání: | 2012 |
Předmět: |
Gene Expression Regulation
Viral Immunology Cattle Diseases Microbiology Dexamethasone Cell Line Mice Virology Alphaherpesvirinae Gene expression Virus latency medicine Animals Promoter Regions Genetic Transcription factor Herpesvirus 1 Bovine Regulation of gene expression biology Promoter Herpesviridae Infections biology.organism_classification medicine.disease Bovine herpesvirus 1 Genome Replication and Regulation of Viral Gene Expression Up-Regulation Virus Latency Cell biology Trigeminal Ganglion Lytic cycle Insect Science Cattle Virus Activation Rabbits hormones hormone substitutes and hormone antagonists Transcription Factors |
Zdroj: | Journal of Virology. 86:2459-2473 |
ISSN: | 1098-5514 0022-538X |
DOI: | 10.1128/jvi.06143-11 |
Popis: | Bovine herpesvirus 1 (BHV-1), an alphaherpesvirinae subfamily member, establishes latency in sensory neurons. Elevated corticosteroid levels, due to stress, reproducibly triggers reactivation from latency in the field. A single intravenous injection of the synthetic corticosteroid dexamethasone (DEX) to latently infected calves consistently induces reactivation from latency. Lytic cycle viral gene expression is detected in sensory neurons within 6 h after DEX treatment of latently infected calves. These observations suggested that DEX stimulated expression of cellular genes leads to lytic cycle viral gene expression and productive infection. In this study, a commercially available assay—Bovine Gene Chip—was used to compare cellular gene expression in the trigeminal ganglia (TG) of calves latently infected with BHV-1 versus DEX-treated animals. Relative to TG prepared from latently infected calves, 11 cellular genes were induced more than 10-fold 3 h after DEX treatment. Pentraxin three, a regulator of innate immunity and neurodegeneration, was stimulated 35- to 63-fold after 3 or 6 h of DEX treatment. Two transcription factors, promyelocytic leukemia zinc finger (PLZF) and Slug were induced more than 15-fold 3 h after DEX treatment. PLZF or Slug stimulated productive infection 20- or 5-fold, respectively, and Slug stimulated the late glycoprotein C promoter more than 10-fold. Additional DEX-induced transcription factors also stimulated productive infection and certain viral promoters. These studies suggest that DEX-inducible cellular transcription factors and/or signaling pathways stimulate lytic cycle viral gene expression, which subsequently leads to successful reactivation from latency in a small subset of latently infected neurons. |
Databáze: | OpenAIRE |
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