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

Frontiers in Cellular and Infection Microbiology

Yongqiang Wang¹  Xiaoqi Li¹  Shijun J. Zheng¹  Bin Wang¹  Yanan Liu¹  Hong Cao¹  Mengjiao Fu¹ 

[1] Department of Preventive Veterinary Medicine, College of Veterinary Medicine, China Agricultural University, Beijing, China;Key Laboratory of Animal Epidemiology of the Ministry of Agriculture, China Agricultural University, Beijing, China;State Key Laboratory of Agrobiotechnology and College of Veterinary Medicine, China Agricultural University, Beijing, China;

关键词: microRNA;    type I IFN;    IBDV;    SOCS;    TANK;   

DOI  :  10.3389/fcimb.2018.00055

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown