Comparative transcriptomic analysis of porcine epidemic diarrhea virus epidemic and classical strains in IPEC-J2 cells.

In recent years, porcine epidemic diarrhea (PED) has become widespread and caused huge economic losses for the global pig industry. There is growing evidence that frequent outbreaks of diarrhea are caused by the variants of porcine epidemic diarrhea virus (PEDV) with high pathogenicity. Herein, an epidemic strain of PEDV HLJ strain was isolated and characterized from Heilongjiang Province of China, and the whole genomic expression profile of intestinal porcine epithelial cells (IPEC-J2) infected with HLJ strain was investigated in comparison with classical CV777 strain. A total of 26,851 genes were identified, of these, 25,880 were known genes and 971 were novel genes. There were 258 differentially expressed genes (DEGs) identified between PEDV HLJ-infected and uninfected cells at 24 h post infection (hpi), and 201 DEGs between PEDV HLJ and CV777 infection. A comparative analysis revealed that 258 DEGs were enriched in 468 gene ontology (GO) terms and mapped to 179 KEGG pathways, and 201 DEGs in 1120 GO terms and mapped to 115 KEGG pathways for HLJ-infected cells in contrast to the uninfected and CV777-infected cells, respectively. Specifically, PEDV HLJ strain could activate anti-viral innate immune response and inflammation more intensively than CV777, in which mRNA levels of interferon (IFN-β), chemokines (CCL5 and CXCL10) and pro-inflammatory cytokines (IL-8 and TNF-α) were induced earlier and more strongly. Subsequently, 20 DEGs and 5 proteins were selected and validated by real-time fluorescence quantitative PCR (RT-qPCR) and western blot, and the results were consistent with the transcriptomic analysis. Overall, this study may be helpful for understanding the pathogenesis mechanism of PEDV variants, and contribute to the effective prevention and control of PEDV infection. • PEDV HLJ strain could adapt and propagate on IPEC-J2 cells with a highest titer of 105.6 TCID 50 at 48 h post infection after serial passages. • The epidemic PEDV HLJ strain, as classified into GI b subgroup, has obvious mutations in its spike and ORF3 protein alignment. • Comparative transcriptomic analysis showed PEDV HLJ strain infection could trigger earlier and stronger responses of inflammation, apoptosis, and innate immunity, in comparison with CV777 strain in cell mitosis and metabolism. This will provide new clues for the further study of the pathogenesis mechanism and PED prevention. [ABSTRACT FROM AUTHOR]