Journal Article
Research Support, Non-U.S. Gov't
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Differential Protein Analysis of IPEC-J2 Cells Infected with Porcine Epidemic Diarrhea Virus Pandemic and Classical Strains Elucidates the Pathogenesis of Infection.

Porcine epidemic diarrhea (PED) re-emerged in China in late 2010 and has now become widespread. Accumulated evidence indicates that this large-scale outbreak of diarrhea was caused by variants of the highly virulent porcine epidemic diarrhea virus (PEDV). A pandemic PEDV YC2014 strain (YC2014) was isolated from clinical samples. An iTRAQ-based comparative quantitative proteomic study of IPEC-J2 cells infected with YC2014 and a classical CV777 strain (CV777) was performed to determine the differences between pandemic and classical PEDV strain infection. Totals of 353 and 299 differentially expressed proteins were identified upon YC2014 and CV777 infection, respectively. The canonical pathways and functional networks involved in both PEDV infections were analyzed. The results indicated that the PEDV suppressed protein synthesis of IPEC-J2 cells through down-regulation of the PI3K-AKT/mTOR signaling pathways. Infection with YC2014 could activate the JAK-STAT signaling pathway and the NF-κB pathway more intensively than CV777. YC2014 could activate NF-κB pathway more intensively than CV777. On the basis of differentially expressed proteins, we propose that PEDV might disrupt apoptosis and may elicit stronger inflammatory cascades as well. This study might contribute to an understanding of the pathogenesis of PEDV infection and aid in the development of effective preventive and control vaccines.

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