Cellular microRNA bta-miR-2361 inhibits bovine herpesvirus 1 replication by directly targeting EGR1 gene

•BHV-1 infection down-regulates bta-miR-2361 expression.•Bta-miR-2361 as a novel host factor regulates BHV-1 replication via directly targeting the EGR1 gene.•BHV-1 infection up-regulates EGR1 expression.•EGR1, as a transcription factor, stimulated viral UL46 promoter activity contributing to BHV-1...

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Bibliographic Details
Published in:Veterinary microbiology 2019-06, Vol.233, p.174-183
Main Authors: Hou, Peili, Zhao, Min, He, Wenqi, He, Hongbin, Wang, Hongmei
Format: Article
Language:English
Subjects:
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Animals
Bioinformatics
Bovidae
Bovine herpesvirus 1 (BHV-1)
Bta-miR-2361
Cattle
Cattle industry
Cell Line
Early growth response 1 (EGR1)
Early Growth Response Protein 1 - genetics
EGR-1 protein
Epithelial Cells
Gene Expression Regulation
Herpesvirus 1, Bovine - pathogenicity
Herpesvirus 1, Bovine - physiology
Host-Pathogen Interactions
Infections
MicroRNAs
MicroRNAs - genetics
miRNA
Pathogenesis
Regulators
Replication
Transfection
UL46
Up-Regulation
Viral Proteins - genetics
Viral replication
Virus Replication
Viruses
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Summary:•BHV-1 infection down-regulates bta-miR-2361 expression.•Bta-miR-2361 as a novel host factor regulates BHV-1 replication via directly targeting the EGR1 gene.•BHV-1 infection up-regulates EGR1 expression.•EGR1, as a transcription factor, stimulated viral UL46 promoter activity contributing to BHV-1 replication.. Bovine herpesvirus 1 (BHV-1) is an economically important pathogen of cattle and has led to significant consequences on the cattle industry worldwide. MicroRNAs (miRNAs) are a class of regulators that play critical roles in virus and host interaction. However, the roles of host miRNAs in BHV-1 infection remain largely unclear. In this study, a set of differentially expressed miRNAs by small RNA deep sequencing were analyzed in the Madin-Darby Bovine Kidney Cells (MDBK) infected with BHV-1 after 12 h, 24 h and 48 h post-infection compared to mock infection, and it was confirmed that bta-miR-2361 was significantly down-regulated. Moreover, bta-miR-2361 mimics transfection could inhibit BHV-1 replication. Combined with up-regulated genes from BHV-1-infected MDBK cells by deep RNA-sequencing and predicted by bioinformatics tools, early growth response 1 (EGR1) was putative target of bta-miR-2361. Furthermore, EGR1 was up-regulated during BHV-1 infection, and overexpression of EGR1 promoted BHV-1 replication whereas knockdown of EGR1 had the opposite effects. Subsequently, the target association between bta-miR-2361 and 3′UTR of EGR1 was further validated using a dual-luciferase reporter assay. In addition, overexpression of bta-miR-2361 resulted in decreased EGR1 mRNA and protein levels. Further mechanistic study showed that EGR1 stimulated BHV-1 UL46 promoter activity, but overexpression of bta-miR-2361 suppressed the production of UL46 gene. Collectively, this is the first study to reveal that bta-miR-2361 as a novel host factor regulates BHV-1 replication via directly targeting the EGR1 gene, which is a transcription factor that regulates viral UL46 gene of BHV-1. These results provide further insight into the study of BHV-1 pathogenesis.
ISSN:0378-1135
1873-2542
DOI:10.1016/j.vetmic.2019.05.004