Original Research ARTICLE
Gga-miR-155 enhances IFN-β expression and suppresses infectious burse disease virus replication via targeting SOCS1 and TANK
- 1China Agricultural University, China
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 IFN-β in DF-1 cells post poly(I:C) stimulation. 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.
Keywords: microRNA, type I IFN, IBDV, SOCS, Tank
Received: 17 Nov 2017;
Accepted: 12 Feb 2018.
Edited by:Santanu Bose, Washington State University, United States
Reviewed by:Alan G. Goodman, Washington State University, United States
Hetron M. Munang'Andu, NMBU, Norway
Hinh Ly, University of Minnesota, United States
Copyright: © 2018 Wang, Liu, Wang, Li, Cao and Zheng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Prof. Shijun Zheng, China Agricultural University, Beijing, China, firstname.lastname@example.org