Abstract

BackgroundPorcine epidemic diarrhea virus (PEDV) is a causative agent of serious viral enteric disease in suckling pigs. Such diseases cause considerable economic losses in the global swine industry. Enhancing our knowledge of PEDV-induced transcriptomic responses in host cells is imperative to understanding the molecular mechanisms involved in the immune response. Here, we analyzed the transcriptomic profile of intestinal porcine epithelial cell line J2 (IPEC-J2) after infection with a classical strain of PEDV to explore the host response.ResultsIn total, 854 genes were significantly differentially expressed after PEDV infection, including 716 upregulated and 138 downregulated genes. Functional annotation analysis revealed that the differentially expressed genes were mainly enriched in the influenza A, TNF signaling, inflammatory response, cytokine receptor interaction, and other immune-related pathways. Next, the putative promoter regions of the 854 differentially expressed genes were examined for the presence of transcription factor binding sites using the MEME tool. As a result, 504 sequences (59.02%) were identified as possessing at least one binding site of signal transducer and activator of transcription (STAT), and five STAT transcription factors were significantly induced by PEDV infection. Furthermore, we revealed the regulatory network induced by STAT members in the process of PEDV infection.ConclusionOur transcriptomic analysis described the host genetic response to PEDV infection in detail in IPEC-J2 cells, and suggested that STAT transcription factors may serve as key regulators in the response to PEDV infection. These results further our understanding of the pathogenesis of PEDV.

Highlights

  • Porcine epidemic diarrhea virus (PEDV) is a causative agent of serious viral enteric disease in suckling pigs

  • Response of intestinal porcine epithelial cell line J2 (IPEC-J2) cells to PEDV strain CV777 infection To detect the effects of PEDV strain CV777 on the growth phenotype of cells, healthy IPEC-J2 cells were infected with CV777 at a multiplicity of infection (MOI) of 1.0

  • Many previous studies have focused on viral isolation and molecular epidemiology surveys [27, 28]; it is necessary to understand the molecular mechanisms involved in the host response to PEDV infection

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Summary

Introduction

Porcine epidemic diarrhea virus (PEDV) is a causative agent of serious viral enteric disease in suckling pigs. Such diseases cause considerable economic losses in the global swine industry. We analyzed the transcriptomic profile of intestinal porcine epithelial cell line J2 (IPEC-J2) after infection with a classical strain of PEDV to explore the host response. PED has resulted in significant economic losses to the pig industry over the past three decades. It was first observed in Europe in 1971 [1]. A more common method of immune prevention is to use infected sow feces and the intestines of infected piglets during pregnancy. The poor external biosecurity of pig farms makes the effectiveness of these preventive methods questionable

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