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Microarray analysis of lncRNA expression in rabies virus infected human neuroblastoma cells

Author:
Ji, Senlin, Zhu, Mengyan, Zhang, Junyan, Cai, Yuchen, Zhai, Xiaofeng, Wang, Dong, Li, Gairu, Su, Shuo, Zhou, Jiyong
Source:
Infection, genetics, and evolution 2019 v.67 pp. 88-100
ISSN:
1567-1348
Subject:
Rabies virus, gene expression regulation, gene ontology, genes, host-pathogen relationships, humans, immune response, messenger RNA, microarray technology, non-coding RNA, pathogenesis, rabies, signal transduction, transcription factors
Abstract:
Rabies, caused by the rabies virus (RABV), is the oldest known zoonotic infectious disease. Although the molecular mechanisms of RABV pathogenesis have been investigated extensively, the interactions between host and RABV are not clearly understood. It is now known that long non-coding RNAs (lncRNAs) participate in various physiological and pathological processes, but their possible roles in the host response to RABV infection remain to be elucidated. To better understand the pathogenesis of RABV, RNAs from RABV-infected and uninfected human neuroblastoma cells (SK-N-SH) were analyzed using human lncRNA microarrays. We identified 896 lncRNAs and 579 mRNAs that were differentially expressed after infection, indicating a potential role for lncRNAs in the immune response to RABV. Differentially expressed RNAs were examined using Gene Ontology (GO) analysis and were tentatively assigned to biological pathways using the Kyoto Encyclopedia of Genes and Genomes (KEGG). A lncRNA-mRNA-transcription factor co-expression network was constructed to relate lncRNAs to regulatory factors and pathways that may be important in virus-host interactions. The network analysis suggests that E2F4, TAF7 and several lncRNAs function as transcriptional regulators in various signaling pathways. This study is the first global analysis of lncRNA and mRNA co-expression during RABV infection, provides deeper insight into the mechanism of RABV pathogenesis, and reveals promising candidate for future investigation.
Agid:
6234647