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miR-155-1 as a positive factor for novel duck reovirus replication by regulating SOCS5-mediated interferons
Diseases caused by novel duck reovirus (NDRV) have brought considerable economic losses to the poultry industry. MicroRNAs (miRNAs) have an impact on virus replication and antiviral immunity. However, the miRNA profile upon NDRV infection in duck embryo fibroblasts (DEFs) remains to be discovered. I...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10194143/ https://www.ncbi.nlm.nih.gov/pubmed/36384170 http://dx.doi.org/10.1016/j.virusres.2022.199003 |
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author | Dong, Yu Yan, Hui Li, Jinman Bei, Lei Shi, Xingxing Zhu, Yanli Xie, Zhijin Zhang, Ruihua Jiang, Shijin |
author_facet | Dong, Yu Yan, Hui Li, Jinman Bei, Lei Shi, Xingxing Zhu, Yanli Xie, Zhijin Zhang, Ruihua Jiang, Shijin |
author_sort | Dong, Yu |
collection | PubMed |
description | Diseases caused by novel duck reovirus (NDRV) have brought considerable economic losses to the poultry industry. MicroRNAs (miRNAs) have an impact on virus replication and antiviral immunity. However, the miRNA profile upon NDRV infection in duck embryo fibroblasts (DEFs) remains to be discovered. In this study, small RNA (sRNA) sequencing was performed to decipher the cellular miRNA response to NDRV infection. Based on 26 differentially expressed miRNAs (19 upregulated and 7 downregulated miRNAs) obtained from sequencing data and their target genes predicted by software, GO and KEGG analyses were performed to elucidate the functions of miRNAs in NDRV invasion, replication, and virus spread. “FoxO signaling pathway”, “autophagy”, and “Toll-like receptor signaling pathway” might participate in NDRV replication as revealed by KEGG enrichment analysis. The miR-155-1 sequence was found to be identical to rno-miR-155-5p and was sharply increased with the progression of NDRV infection. Moreover, NDRV-induced miR-155-1 could act as a positive factor for virus replication in DEFs, which inhibited type I interferon (IFN-I) production. Luciferase assay confirmed that miR-155-1 disturbed the abundance of suppressor of cytokine signaling (SOCS) 5 by targeting 3’-UTR. SOCS5, which is linked to increased IRF7 expression, restricts IFN expression and promotes NDRV replication in DEFs. Therefore, this study proposed that miR-155-1 was used by NDRV to restrict SOCS5 expression, attenuating the production of IFN-I and creating a favorable environment for virus replication. |
format | Online Article Text |
id | pubmed-10194143 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-101941432023-05-19 miR-155-1 as a positive factor for novel duck reovirus replication by regulating SOCS5-mediated interferons Dong, Yu Yan, Hui Li, Jinman Bei, Lei Shi, Xingxing Zhu, Yanli Xie, Zhijin Zhang, Ruihua Jiang, Shijin Virus Res Article Diseases caused by novel duck reovirus (NDRV) have brought considerable economic losses to the poultry industry. MicroRNAs (miRNAs) have an impact on virus replication and antiviral immunity. However, the miRNA profile upon NDRV infection in duck embryo fibroblasts (DEFs) remains to be discovered. In this study, small RNA (sRNA) sequencing was performed to decipher the cellular miRNA response to NDRV infection. Based on 26 differentially expressed miRNAs (19 upregulated and 7 downregulated miRNAs) obtained from sequencing data and their target genes predicted by software, GO and KEGG analyses were performed to elucidate the functions of miRNAs in NDRV invasion, replication, and virus spread. “FoxO signaling pathway”, “autophagy”, and “Toll-like receptor signaling pathway” might participate in NDRV replication as revealed by KEGG enrichment analysis. The miR-155-1 sequence was found to be identical to rno-miR-155-5p and was sharply increased with the progression of NDRV infection. Moreover, NDRV-induced miR-155-1 could act as a positive factor for virus replication in DEFs, which inhibited type I interferon (IFN-I) production. Luciferase assay confirmed that miR-155-1 disturbed the abundance of suppressor of cytokine signaling (SOCS) 5 by targeting 3’-UTR. SOCS5, which is linked to increased IRF7 expression, restricts IFN expression and promotes NDRV replication in DEFs. Therefore, this study proposed that miR-155-1 was used by NDRV to restrict SOCS5 expression, attenuating the production of IFN-I and creating a favorable environment for virus replication. Elsevier 2022-11-13 /pmc/articles/PMC10194143/ /pubmed/36384170 http://dx.doi.org/10.1016/j.virusres.2022.199003 Text en © 2022 The Authors. Published by Elsevier B.V. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Article Dong, Yu Yan, Hui Li, Jinman Bei, Lei Shi, Xingxing Zhu, Yanli Xie, Zhijin Zhang, Ruihua Jiang, Shijin miR-155-1 as a positive factor for novel duck reovirus replication by regulating SOCS5-mediated interferons |
title | miR-155-1 as a positive factor for novel duck reovirus replication by regulating SOCS5-mediated interferons |
title_full | miR-155-1 as a positive factor for novel duck reovirus replication by regulating SOCS5-mediated interferons |
title_fullStr | miR-155-1 as a positive factor for novel duck reovirus replication by regulating SOCS5-mediated interferons |
title_full_unstemmed | miR-155-1 as a positive factor for novel duck reovirus replication by regulating SOCS5-mediated interferons |
title_short | miR-155-1 as a positive factor for novel duck reovirus replication by regulating SOCS5-mediated interferons |
title_sort | mir-155-1 as a positive factor for novel duck reovirus replication by regulating socs5-mediated interferons |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10194143/ https://www.ncbi.nlm.nih.gov/pubmed/36384170 http://dx.doi.org/10.1016/j.virusres.2022.199003 |
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