Identification of the IFN-β response in H3N2 canine influenza virus infection.
Canine influenza viruses (CIVs) circulate continuously in the dog population, providing opportunities for exposure to humans and other species. Although the dog genome has been sequenced, innate immunity in dogs is not well characterized, which limits the understanding of H3N2 canine influenza virus pathogenesis. Equally, how this virus evades the canine host innate immune response to successfully establish infection remains unclear. To analyse the IFN-β response to CIV infection in Madin-Darby canine kidney cells, the canine IFN-β promoter sequence and its positive regulatory domain motifs were first cloned and identified using a luciferase reporter system. Next, we found that infection with the CIV strain GD/12 blocked the IFN-β response primarily by inhibiting the NF-κB and IFN regulatory factor 3 (IRF3) signalling pathways. Expression of GD/12 non-structural protein 1 alone was sufficient to inhibit Sendai virus-induced NF-κB and IRF3 activation by suppressing p65 and IRF3 phosphorylation, suggesting the important role of this protein in the CIV-mediated inhibition of the IFN-β response. These results suggest that inhibition of the IFN-β signalling pathway may have played a role in CIV establishment and spread in dog populations.
College of Veterinary Medicine, South China Agricultural University, Guangzhou, PR China.|Key Laboratory of Comprehensive Prevention and Control for Severe Clinical Animal Diseases of Guangdong Province, Guangzhou, PR China.|Guangdong Engineering and Technological Research Center on pet, Guangzhou, PR China.
Shuo
S
Su
College of Veterinary Medicine, South China Agricultural University, Guangzhou, PR China.|Key Laboratory of Comprehensive Prevention and Control for Severe Clinical Animal Diseases of Guangdong Province, Guangzhou, PR China.|Guangdong Engineering and Technological Research Center on pet, Guangzhou, PR China.
San
S
Huang
College of Veterinary Medicine, South China Agricultural University, Guangzhou, PR China.|Key Laboratory of Comprehensive Prevention and Control for Severe Clinical Animal Diseases of Guangdong Province, Guangzhou, PR China.|Guangdong Engineering and Technological Research Center on pet, Guangzhou, PR China.
Cheng
C
Fu
College of Veterinary Medicine, South China Agricultural University, Guangzhou, PR China.|Key Laboratory of Comprehensive Prevention and Control for Severe Clinical Animal Diseases of Guangdong Province, Guangzhou, PR China.|Guangdong Engineering and Technological Research Center on pet, Guangzhou, PR China.
Lifang
L
Wang
College of Veterinary Medicine, South China Agricultural University, Guangzhou, PR China.|Key Laboratory of Comprehensive Prevention and Control for Severe Clinical Animal Diseases of Guangdong Province, Guangzhou, PR China.|Guangdong Engineering and Technological Research Center on pet, Guangzhou, PR China.
Yun
Y
Zheng
College of Veterinary Medicine, South China Agricultural University, Guangzhou, PR China.|Key Laboratory of Comprehensive Prevention and Control for Severe Clinical Animal Diseases of Guangdong Province, Guangzhou, PR China.|Guangdong Engineering and Technological Research Center on pet, Guangzhou, PR China.
Pei
P
Zhou
College of Veterinary Medicine, South China Agricultural University, Guangzhou, PR China.|Key Laboratory of Comprehensive Prevention and Control for Severe Clinical Animal Diseases of Guangdong Province, Guangzhou, PR China.|Guangdong Engineering and Technological Research Center on pet, Guangzhou, PR China.
Shoujun
S
Li
D000818:Animals; D004285:Dogs; D054884:Host-Pathogen Interactions; D053122:Influenza A Virus, H3N2 Subtype / Q000276:immunology* / Q000302:isolation & purification; D016899:Interferon-beta / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D061985:Madin Darby Canine Kidney Cells; D008962:Models, Theoretical; D015398:Signal Transduction
D016899:Interferon-beta