Analysis of lncRNA Expression Profiles in DF-1 Cells Infected with Infectious bursal disease virus (IBDV)
DING Ying-Nan1, YU Tian-Qi1, ZHANG Yi-Na2, ZHOU Ji-Yong2, HU Bo-Li1,*
1 MOE Joint International Research Laboratory of Animal Health and Food Safety/Institute of Immunology, Nanjing Agricultural University, Nanjing 210095, China; 2 MOA Key Laboratory of Animal Virology/Department of Veterinary Medicine, Zhejiang University, Hangzhou 310058, China
Abstract Infectious bursal disease (IBD) is an acute, highly contagious infectious disease caused by Infectious bursal disease virus (IBDV). The incidence rate of IBD in susceptible young chickens (Gallus gallus)can reach 80%~100%, and the mortality rate is as high as 30%~35%. To test the changes of long noncoding RNA (lncRNA) in host cells infected with IBDV, the expression profile of lncRNA in IBDV-infected and mock-infected chicken fibroblast line DF-1 cells were analyzed by high throughput sequencing. The results showed that there were 958 differentially expressed lncRNA. Among them, 728 were up-regulated and 230 were down-regulated. Target genes of the differentially expressed lncRNA were predicted. Functional annotation or enrichment analysis was performed by Gene Oncology (GO) or Kyoto Encyclopedia of Genes and Genomes (KEGG). GO analysis suggested that target genes of the differentially expressed lncRNA involved in immune response, cell death, response to cytokine and I-κB kinase/NF-κB signaling. KEGG enrichment analysis suggested that these genes functioned in various cellular signaling pathways, including Toll-like receptor signaling pathway, RIG-I-like receptor signaling pathway and apoptosis. Differentially expression of 9 randomly selected lncRNAs were verified by real-time quantitative polymerase chain reaction (qRT-PCR). The results were consistent with high throughput sequencing data. This is the first report of the differentially expression of lncRNA in DF-1 cells upon IBDV infection. This study provides a basis for further research on key lncRNA related to the host immunity and IBDV pathogenesis.
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