Abstract

Duck is a major waterfowl species in China, providing high-economic benefit with a population of up to 20–30 billion per year. Ducks are commonly affected by severe diseases, including egg-drop syndrome caused by duck Tembusu virus (DTMUV). The immune mechanisms against DTMUV invasion and infection remain poorly understood. In this study, duck embryo fibroblasts (DEFs) were infected with DTMUV and harvested at 12 and 24 h post-infection (hpi), and their genomes were sequenced. In total, 911 (764 upregulated and 147 downregulated genes) and 3008 (1791 upregulated and 1217 downregulated) differentially expressed genes (DEGs) were identified at 12 and 24 hpi, respectively. Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that DEGs were considerably enriched in immune-relevant pathways, including Toll-like receptor signaling pathway, Cytosolic DNA-sensing pathway, RIG-I-like receptor signaling pathway, Chemokine signaling pathway, NOD-like receptor signaling pathway, and Hematopoietic cell lineage at both time points. The key DEGs in immune system included those of the cytokines (IFN α2, IL-6, IL-8L, IL-12B, CCR7, CCL19, and CCL20), transcription factors or signaling molecules (IRF7, NF-κB, STAT1, TMEM173, and TNFAIP3), pattern recognition receptors (RIG-I and MDA5), and antigen-presenting proteins (CD44 and CD70). This suggests DTMUV infection induces strong proinflammatory/antiviral effects with enormous production of cytokines. However, these cytokines could not protect DEFs against viral attack. Our data revealed valuable transcriptional information regarding DTMUV-infected DEFs, thereby broadening our understanding of the immune response against DTMUV infection; this information might contribute in developing strategies for controlling the prevalence of DTMUV infection.

Highlights

  • Hemorrhagic ovarian inflammation, termed egg-drop syndrome, is primarily caused by duck Tembusu virus (DTMUV), and has resulted in significant economic losses in the poultry industry in Southeast Asia since 2010 [1]

  • A wide spectrum of mammalian cells exhibit cytopathic effects (CPEs) following Tembusu virus infection, such as A549, BHK21, Hela, Vero, and SH-SY5Y [10], and including HEK293 according to our recent study

  • In cells infected with DTMUV, CPEs were observed as early as 24 hpi (Figure 1d)

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Summary

Introduction

Hemorrhagic ovarian inflammation, termed egg-drop syndrome, is primarily caused by duck Tembusu virus (DTMUV), and has resulted in significant economic losses in the poultry industry in Southeast Asia since 2010 [1]. A wide spectrum of mammalian cells exhibit cytopathic effects (CPEs) following Tembusu virus infection, such as A549, BHK21, Hela, Vero, and SH-SY5Y [10], and including HEK293 according to our recent study. These findings imply that the virus has expanded its host range and may pose a threat to mammals’ health [11]

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