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Borna disease virus 1 (BoDV-1) is neurotropic prototype of Bornaviruses causing neurological diseases and maintaining persistent infection in brain cells of mammalian species. Long non-coding RNA (lncRNA) is transcript of more than 200 nucleotides without protein-coding function regulating various biological processes as proliferation, apoptosis, cell migration and viral infection. However, regulatory of lncRNAs in BoDV-1 infection remains unknown. To identify differential expression profiles and predict functions of lncRNA in BoDV-1 infection, microarray data showed that 3528 lncRNAs and 2661 lncRNAs were differentially expressed in Strain V and Hu-H1 BoDV-infected groups compared with control groups, respectively. Gene Ontology (GO) and pathway analysis suggested that differential lncRNAs may be involved in regulation of metabolic, biological regulation, cellular process, endocytosis, viral infections and cell adhesion processes, cancer in both BoDV-infected strains. ENSMUST00000128469 was found down-regulated in both BoDV-infected groups compared with control groups consistent with microarray (p < 0.05). ceRNA analysis indicated possible interaction networks as ENSMUST00000128469/miR-22-5p, miR-206-3p, miR-302b-5p, miR-302c-3p, miR-1a-3p/Igf1. Igf1 was found up-regulated in both BoDV-infected groups compared with control groups (p < 0.05). Possible functions of predicted target mRNAs and miRNAs of ENSMUST00000128469 were involved in cell proliferation, transcriptional misregulation and proteoglycan pathways enriched in cancer. lncRNA may be involved in regulation of Hu-H1 inhibited cell proliferation and promoted apoptosis through NF-kB, JNK/MAPK signaling, BCL2 and CDK6/E2F1 pathways different from Strain V. Possible interaction networks as ENSMUST00000128469/miR-22-5p, miR-206-3p, miR-302b-5p, miR-302c-3p, miR-1a-3p/Igf1 may involve in regulation of cell proliferation, apoptosis, and cancer.

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Publication history

Received: 20 December 2018
Accepted: 09 April 2019
Published: 17 April 2019
Issue date: June 2019

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© 2019, Chongqing Medical University.

Acknowledgements

Acknowledgements

We thank Professor Hanns Ludwig, Berlin Free University, Germany, and Dr. Liv Bode, Robert Koch Institute, Germany, for providing BoDV strain Hu-H1 and Strain V. This work was supported by the National Key Research and Development Program of China, China (Grant No. YFA0505700) and the Natural Science Foundation of China, China (Grant No.81601207).

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This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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