Bta-miR-2890 up-regulates JAK-STAT pathway to inhibit BoHV-1 replication by targeting viral gene UL41

  • Vet Microbiol. 2020 Jun;245:108709. doi: 10.1016/j.vetmic.2020.108709.
Wenqing Ma  1 ,  Hongmei Wang  2 ,  Hongbin He  3
Affiliations
  • 1. Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, P. R. China.
  • 2. Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, P. R. China. Electronic address: [email protected].
  • 3. Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, 250014, P. R. China. Electronic address: [email protected].
PMID: 32456827 DOI: 10.1016/j.vetmic.2020.108709
Abstract

MicroRNAs have emerged as important and versatile modulators of immune responses and participate actively in the regulation of host-pathogen interactions. However, the role of miR-2890 in the host response against viral Infection is unclear. In this study, we show that bta-miR-2890 facilitates the production of type I interferon (IFN) and IFN-stimulated genes, and inhibits bovine alphaherpesvirus 1 (BoHV-1) replication. Further research showed that bta-miR-2890 actives the type I IFN signal pathway via up-regulating JAK1 and STAT1 by directly targeting BoHV-1 UL41 3'UTR. Here, we found that BoHV-1 UL41 inhibits JAK1 expression. Mechanistically, BoHV-1 UL41 up-regulates E3 ubiquitin Ligase SYVN1, which promotes K48-linked polyubiquitination and proteasomal degradation of JAK1. Together, our results suggest that bta-miR-2890 promotes JAK1 and STAT1 expression via targeting BoHV-1 UL41 is an important event for IFN-dependent Antiviral immune response, and suggest that bta-miR-2890 has an important role in controlling viral infections.

Keywords
BoHV-1; JAK1-STAT; UL41; bta-miR-2890.
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