ABSTRACT

The functions and profiles of lncRNAs during infectious bursal disease virus (IBDV) infection have not been determined, yet. The objectives of this study were to determine the antiviral action of loc107051710 lncRNA during IBDV infection by investigating the relationship between loc107051710 and IRF8, Type I IFN, STATs, and ISGs. DF-1 cells were either left untreated as non-infected controls (n = 1) or infected with IBDV (n = 3). RNA sequencing was applied for analysis of mRNAs and lncRNAs expression. Differentially expressed genes were verified by RT-qPCR. Then identification, of 230 significantly different expressed genes (182 mRNAs and 48 lncRNA) by pairwise comparison of the infected and control groups, was carried out. The functions of differentially expressed lncRNAs were investigated by selection of lncRNAs and mRNAs significantly enriched in the aforementioned biological processes and signaling pathways for construction of lncRNA-mRNA co-expression networks. The techniques of gene ontology and Kyoto Encyclopedia of Genes and Genomes pathways were applied. It was suggested that these differentially expressed genes were involved in the interaction between the host and IBDV. Loc107051710 was found to have potential antiviral effects. RT-qPCR and western blot were applied and revealed that loc107051710 was required for induction of IRF8, type I IFN, STAT, and ISG expression, and its knockdown promoted IBDV replication. By fluorescence in situ hybridization, it was found that loc107051710 was translocated from the nucleus to the cytoplasm after infection with IBDV. Overall, loc107051710 promoted the production of IFN-α and IFN-β by regulating IRF8, thereby promoting the antiviral activity of ISGs.

摘要

尚未确定lncRNA在传染性法氏囊病病毒（IBDV）感染过程中的功能和概况。这项研究的目的是通过调查loc107051710与IRF8，I型IFN，STAT和ISG之间的关系，确定IBDV感染中loc107051710 lncRNA的抗病毒作用。DF-1细胞要么未经处理就作为未感染的对照（n = 1），要么被IBDV感染（n = 3）。RNA测序用于分析mRNA和lncRNA的表达。通过RT-qPCR验证差异表达的基因。然后通过成对比较感染和对照组，鉴定了230个显着不同的表达基因（182个mRNA和48个lncRNA）。通过选择在上述生物学过程和信号通路中显着丰富的lncRNA和mRNA的选择来研究差异表达的lncRNA的功能，以构建lncRNA-mRNA共表达网络。应用了基因本体技术和《京都议定书》中的基因与基因组途径。提示这些差异表达的基因参与了宿主与IBDV之间的相互作用。发现Loc107051710具有潜在的抗病毒作用。应用了RT-qPCR和western blot，结果表明loc107051710是诱导IRF8，I型IFN，STAT和ISG表达所必需的，其敲低促进了IBDV复制。通过荧光原位杂交，发现在用IBDV感染后，loc107051710从细胞核转移到细胞质。总体而言，loc107051710通过调节IRF8促进了IFN-α和IFN-β的产生，从而促进了ISG的抗病毒活性。