Global and quantitative proteomic analysis of dogs infected by avian-like H3N2 canine influenza virus

Abstract

Canine influenza virus A (H3N2) is a newly emerged etiological agent for respiratory infections in dogs. The mechanism of interspecies transmission from avian to canine species and the development of diseases in this new host remain to be explored. To investigate this, we conducted a differential proteomics study in 2-month-old beagles inoculated intranasally with 106 TCID50 of A/canine/Guangdong/01/2006 (H3N2) virus. Lung sections excised at 12 h post-inoculation (hpi), 4 days, and 7 days post-inoculation (dpi) were processed for global and quantitative analysis of differentially expressed proteins. A total of 17,796 proteins were identified at different time points. About 1.6% was differentially expressed between normal and infected samples. Of these, 23, 27, and 136 polypeptides were up-regulated, and 14, 18, and 123 polypeptides were down-regulated, at 12 hpi, 4 dpi, and 7 dpi, respectively. Vann diagram analysis indicated that 17 proteins were up-regulated and one was down-regulated at all three time points. Selected proteins were validated by real-time PCR and by Western blot. Our results show that apoptosis and cytoskeleton-associated proteins expression was suppressed, whereas interferon-induced proteins plus other innate immunity proteins were induced after the infection. Understanding of the interactions between virus and the host will provide insights into the basis of interspecies transmission, adaptation, and virus pathogenicity.

Proteomics Analysis of Differential Expression of Lung Proteins in Response to Highly Pathogenic Avian Influenza Virus Infection in Chicken

“…Cytoskeletal proteins have been reported to interact with viral proteins to regulate viral replication and assembly as well as the transport of viral components in the cell (Avalos et al, 1997; Radtke et al, 2006). Similar associations of cytoskeletal proteins with influenza infection condition are also reported previously (Coombs et al, 2010; Sui et al, 2014; Su et al, 2015). The cyclin-dependent kinases (CDKs) such as CDK13, DDB1, DRD3, FOXG1, and TCF3 that are involved in the regulation of cell cycle were all upregulated in chicken lung proteome.…”

“…Protein kinase activity associated proteins, namely, JAK3, MARK3, TBK1, EIF2AK3, PRKCA, and TRPM6were downregulated in the chicken lung tissues. Differential expression of proteins including signal transduction molecules, kinases and other biochemical metabolism related enzymes that are associated with the repair of damaged lung tissues are reported in dogs infected with influenza virus infection (Su et al, 2015). In addition, some apoptosis and tumor-associated proteins (BCL6, FAF1, TBX5, AKAP13, TNFSF10 and TGFB1) were also identified in the chicken lung proteome.…”

“…Proteomics studies of influenza virus infection in macaques (Brown et al, 2010), mice (Kumar et al, 2014), continuous cell lines (Vester et al, 2009; Coombs et al, 2010; Kummer et al, 2014), chicken (Zou et al, 2010; Li et al, 2017), dogs (Su et al, 2015) and primary human cells (Liu et al, 2008; Lietzen et al, 2011; Kroeker et al, 2012; Liu et al, 2012) have provided information on alteration of host proteome at cellular and organism levels. Recent studies of chicken proteome response against H5N1 infection revealed several alterations of cytoskeleton, metabolic process, cellular component, and transcription regulation proteins (Zou et al, 2010; Li et al, 2017).…”

Role of CARD Region of MDA5 Gene in Canine Influenza Virus Infection

“…Primers are shown in Table 2. Poly I:C was transfected as a positive control into MDCK cells using Lipofectamine 3000 (Invitrogen) [40,41]. p3xFLAG-MDA5, p3xFLAG-MDA5-CARD, and p3xFLAG were transiently transfected into MDCK cells using Lipofectamine 3000 (Invitrogen).…”

The NS1 protein of H5N6 feline influenza virus inhibits feline beta interferon response by preventing NF-κB and IRF3 activation

“…Wild birds are probably the most important natural reservoir hosts of IAVs as they maintain a vast viral gene pool and pose a continuous threat to humans and other mammalian species (Yoon et al, 2014). Agricultural practices and ecological systems in China and other eastern Asian countries have provided ample opportunities for avian influenza viruses (AIVs) to cross species barriers and cause sporadic infections in mammals (Su et al, 2014a(Su et al, , 2014b(Su et al, , 2015a(Su et al, , 2015b). An AIV of the H5N6 subtype was responsible for a recent outbreak amongst birds in Laos, Vietnam, and China that resulted in the culling of~100,000 chickens Guillaume Belot et al, 2014;Qi et al, 2014;Shen et al, 2015;Wong et al, 2015;Wu et al, 2015a).…”