4.4 Article

Analysis of the long noncoding RNA profiles of RD and SH-SY5Y cells infected with coxsackievirus B5, using RNA sequencing

Journal

ARCHIVES OF VIROLOGY
Volume 167, Issue 2, Pages 367-376

Publisher

SPRINGER WIEN
DOI: 10.1007/s00705-021-05313-6

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Funding

  1. National Natural Science Foundation of China [81860357]
  2. Young Talents Support Program of Yunnan Province (Ten Thousand People Plan) [YNWRQNBJ-2019-178]
  3. State Key Laboratory of Virology [2018KF006]

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The study revealed differential expression of lncRNAs in CV-B5-infected RD and SH-SY5Y cells, with implications in disease and signaling pathways, suggesting the potential therapeutic use of lncRNAs as novel molecular targets for CV-B5 infection and neurogenic diseases caused by it.
Hand, foot, and mouth disease caused by coxsackievirus B5 (CV-B5) is a considerable threat to infant health, especially with regard to neurological damage. Long noncoding RNAs (lncRNAs) are known to play pivotal roles in virus-host interactions. However, the roles of lncRNAs in CV-B5-host interactions have not yet been elucidated. In the current study, we used RNA sequencing to determine the expression profiles of lncRNAs in CV-B5-infected human rhabdomyosarcoma (RD) and SH-SY5Y cells. Our results showed that, of the differentially expressed lncRNAs, 508 were upregulated and 760 were downregulated in RD cells. Of these, 46.2% were long noncoding intergenic RNAs (lincRNAs), 28.6% were antisense lncRNAs, 24.1% were sense overlapping lncRNAs, and 1.0% were sense intronic lncRNAs. Moreover, 792 lncRNAs were upregulated and 811 lncRNAs were downregulated in SH-SY5Y cells, 48.6% of which were lincRNAs, 34.7% were antisense lncRNAs, 16.0% were sense overlapping lncRNAs, and 0.8% were sense intronic lncRNAs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that lncRNAs that were differentially expressed in CV-B5-infected RD cells were associated with disease, and those differentially expressed in SH-SY5Y cells were involved in signaling pathways. RT-qPCR analysis of seven lncRNAs supported these results. Moreover, our study revealed that lncRNA-IL12A inhibits viral replication. We conclude that lncRNAs constitute potential novel molecular targets for the prevention and treatment of CV-B5 infection and also may serve to distinguish neurogenic diseases caused by CV-B5 infection.

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