Frontiers in Cellular and Infection Microbiology (Mar 2018)

gga-miR-155 Enhances Type I Interferon Expression and Suppresses Infectious Burse Disease Virus Replication via Targeting SOCS1 and TANK

  • Bin Wang,
  • Bin Wang,
  • Bin Wang,
  • Mengjiao Fu,
  • Mengjiao Fu,
  • Mengjiao Fu,
  • Yanan Liu,
  • Yanan Liu,
  • Yanan Liu,
  • Yongqiang Wang,
  • Yongqiang Wang,
  • Yongqiang Wang,
  • Xiaoqi Li,
  • Hong Cao,
  • Hong Cao,
  • Hong Cao,
  • Shijun J. Zheng,
  • Shijun J. Zheng,
  • Shijun J. Zheng

DOI
https://doi.org/10.3389/fcimb.2018.00055
Journal volume & issue
Vol. 8

Abstract

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Infectious bursal disease (IBD) is an acute, highly contagious, and immunosuppressive avian disease caused by IBD virus (IBDV). MicroRNAs (miRNAs) are involved in host-pathogen interactions and innate immune response to viral infection. However, the role of miRNAs in host response to IBDV infection is not clear. We report here that gga-miR-155 acts as an anti-virus host factor inhibiting IBDV replication. We found that transfection of DF-1 cells with gga-miR-155 suppressed IBDV replication, while blockage of the endogenous gga-miR-155 by inhibitors enhanced IBDV replication. Furthermore, our data showed that gga-miR-155 enhanced the expression of type I interferon in DF-1 cells post IBDV infection. Importantly, we found that gga-miR-155 enhanced type I interferon expression via targeting SOCS1 and TANK, two negative regulators of type I IFN signaling. These results indicate that gga-miR-155 plays a critical role in cell response to IBDV infection.

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