4.4 Article

Comparison of lncRNA and mRNA expression in mouse brains infected by a wild-type and a lab-attenuated Rabies lyssavirus

期刊

JOURNAL OF GENERAL VIROLOGY
卷 102, 期 3, 页码 -

出版社

MICROBIOLOGY SOC
DOI: 10.1099/jgv.0.001538

关键词

Rabies lyssavirus; RNA-seq; long non-coding RNA; immune responses

资金

  1. National Program on Key Research Project of China [2016YFD0500400]
  2. Fundamental Research Funds for the Central Universities [2662015PY227]
  3. National Natural Science Foundation of China [31872451]

向作者/读者索取更多资源

The study identified differentially expressed lncRNAs and mRNAs in wild-type and lab-attenuated RABV-infected mouse brains, revealing their association with immune response and ion transport-related pathways, providing insights into the potential role of lncRNA in immune evasion and neuron injury induced by WT RABV.
Rabies is a lethal disease caused by Rabies lyssavirus, commonly known as rabies virus (RABV), and results in nearly 100 % death once clinical symptoms occur in human and animals. Long non-coding RNAs (lncRNAs) have been reported to be associated with viral infection. But the role of lncRNAs involved in RABV infection is still elusive. In this study, we performed global transcriptome analysis of both of lncRNA and mRNA expression profiles in wild-type (WT) and lab-attenuated RABV-infected mouse brains by using next-generation sequencing. The differentially expressed lncRNAs and mRNAs were analysed by using the edgeR package. We identified 1422 differentially expressed lncRNAs and 4475 differentially expressed mRNAs by comparing WT and lab-attenuated RABV-infected brains. Then we predicted the enriched biological pathways by the Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) database based on the differentially expressed lncRNAs and mRNAs. Our analysis revealed the relationships between lncRNAs and RABV-infection-associated immune response and ion transport-related pathways, which provide a fresh insight into the potential role of lncRNA in immune evasion and neuron injury induced by WT RABV.

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