Open AccessIdentification of the IFN-β response in H3N2 canine influenza virus infection
Author(s) -
Shuo Su,
Huang San,
Cheng Fu,
Lifang Wang,
Yun Zheng,
Pei Zhou
Publication year - 2016
Publication title -
journal of general virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.55
H-Index - 167
eISSN - 1465-2099
pISSN - 0022-1317
DOI - 10.1099/jgv.0.000322
Subject(s) - biology , sendai virus , irf3 , virology , innate immune system , virus , influenza a virus , pathogenesis , population , immune system , immunology , demography , sociology
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.