Frontiers in Veterinary Science (Dec 2020)

Phosphoproteomics to Characterize Host Response During H3N2 Canine Influenza Virus Infection of Dog Lung

  • Yongbo Liu,
  • Yongbo Liu,
  • Yongbo Liu,
  • Cheng Fu,
  • Shaotang Ye,
  • Shaotang Ye,
  • Shaotang Ye,
  • Yingxin Liang,
  • Yingxin Liang,
  • Yingxin Liang,
  • Zhonghe Qi,
  • Zhonghe Qi,
  • Zhonghe Qi,
  • Congwen Yao,
  • Congwen Yao,
  • Congwen Yao,
  • Zhen Wang,
  • Zhen Wang,
  • Zhen Wang,
  • Ji Wang,
  • Ji Wang,
  • Ji Wang,
  • Siqi Cai,
  • Siqi Cai,
  • Siqi Cai,
  • Shiyu Tang,
  • Shiyu Tang,
  • Shiyu Tang,
  • Ying Chen,
  • Ying Chen,
  • Ying Chen,
  • Shoujun Li,
  • Shoujun Li,
  • Shoujun Li

DOI
https://doi.org/10.3389/fvets.2020.585071
Journal volume & issue
Vol. 7

Abstract

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Avian-origin H3N2 canine influenza viruses (CIVs) cause severe contagious respiratory disease in dogs, and quickly adapt to new environments. To further understand the mechanism of virus infection and host-virus interactions, we characterized the complete phosphoproteome of dogs infected with H3N2 CIV. Nine-week-old Beagle dogs were inoculated intranasally with 106 EID50 of A/canine/Guangdong/04/2014 (H3N2) virus. Lung sections were harvested at 5 days post-inoculation (dpi) and processed for global and quantitative analysis of differentially expressed phosphoproteins. A total of 1,235 differentially expressed phosphorylated proteins were identified in the dog lung after H3N2 CIV infection, and 3,016 modification sites were identified among all differentially expressed proteins. We then performed an enrichment analysis of functional annotations using Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene ontology (GO) database analyses to predict the functions of the identified differential phosphoproteins. Our data indicate that H3N2 CIV infection causes dramatic changes in the host protein phosphorylation of dog lungs. To our knowledge, this is the first study to assess the effect of H3N2 CIV infection on the phosphoproteome of beagles. These data provide novel insights into H3N2-CIV-triggered regulatory phosphorylation circuits and signaling networks and may improve our understanding of the mechanisms underlying CIV pathogenesis in dogs.

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