gga-miR-155 Enhances Type I Interferon Expression and Suppresses Infectious Burse Disease Virus Replication via Targeting SOCS1 and TANK.
Front Cell Infect Microbiol
; 8: 55, 2018.
Article
in En
| MEDLINE
| ID: mdl-29564226
ABSTRACT
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.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Interferon Type I
/
Infectious bursal disease virus
/
MicroRNAs
/
Adaptor Proteins, Signal Transducing
/
Host-Pathogen Interactions
/
Suppressor of Cytokine Signaling 1 Protein
Limits:
Animals
Language:
En
Journal:
Front Cell Infect Microbiol
Year:
2018
Document type:
Article
Affiliation country:
China