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Identification of pathogenic genes and transcription factors in respiratory syncytial virus
BACKGROUND: Respiratory syncytial virus (RSV) is a major cause of acute lower respiratory infections in children, especially bronchiolitis. Our study aimed to identify the key genes and upstream transcription factors in RSV. METHODS: To screen for RSV pathogenic genes, an integrated analysis was per...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7796524/ https://www.ncbi.nlm.nih.gov/pubmed/33419394 http://dx.doi.org/10.1186/s12887-020-02480-4 |
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author | Li, Lei Ni, Yong An Song, Zhenfeng Yi, Zhi Wang, Fang |
author_facet | Li, Lei Ni, Yong An Song, Zhenfeng Yi, Zhi Wang, Fang |
author_sort | Li, Lei |
collection | PubMed |
description | BACKGROUND: Respiratory syncytial virus (RSV) is a major cause of acute lower respiratory infections in children, especially bronchiolitis. Our study aimed to identify the key genes and upstream transcription factors in RSV. METHODS: To screen for RSV pathogenic genes, an integrated analysis was performed using the RSV microarray dataset in GEO. Functional annotation and potential pathways for differentially expressed genes (DEGs) were further explored by GO and KEGG enrichment analysis. We constructed the RSV-specific transcriptional regulatory network to identify key transcription factors for DEGs in RSV. RESULTS: From three GEO datasets, we identified 1059 DEGs (493 up-regulated and 566 down-regulated genes, FDR < 0.05 and |Combined.ES| > 0.8) between RSV patients and normal controls. GO and KEGG analysis revealed that ‘response to virus’ (FDR = 7.13E-15), ‘mitochondrion’ (FDR = 1.39E-14) and ‘Asthma’ (FDR = 1.28E-06) were significantly enriched pathways for DEGs. The expression of IFI27, IFI44, IFITM3, FCER1A, and ISG15 were shown to be involved in the pathogenesis of RSV. CONCLUSIONS: We concluded that IFI27, IFI44, IFITM3, FCER1A, and ISG15 may play a role in RSV. Our finding may contribute to the development of new potential biomarkers, reveal the underlying pathogenesis and also identify novel therapeutic targets for RSV. |
format | Online Article Text |
id | pubmed-7796524 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-77965242021-01-11 Identification of pathogenic genes and transcription factors in respiratory syncytial virus Li, Lei Ni, Yong An Song, Zhenfeng Yi, Zhi Wang, Fang BMC Pediatr Research Article BACKGROUND: Respiratory syncytial virus (RSV) is a major cause of acute lower respiratory infections in children, especially bronchiolitis. Our study aimed to identify the key genes and upstream transcription factors in RSV. METHODS: To screen for RSV pathogenic genes, an integrated analysis was performed using the RSV microarray dataset in GEO. Functional annotation and potential pathways for differentially expressed genes (DEGs) were further explored by GO and KEGG enrichment analysis. We constructed the RSV-specific transcriptional regulatory network to identify key transcription factors for DEGs in RSV. RESULTS: From three GEO datasets, we identified 1059 DEGs (493 up-regulated and 566 down-regulated genes, FDR < 0.05 and |Combined.ES| > 0.8) between RSV patients and normal controls. GO and KEGG analysis revealed that ‘response to virus’ (FDR = 7.13E-15), ‘mitochondrion’ (FDR = 1.39E-14) and ‘Asthma’ (FDR = 1.28E-06) were significantly enriched pathways for DEGs. The expression of IFI27, IFI44, IFITM3, FCER1A, and ISG15 were shown to be involved in the pathogenesis of RSV. CONCLUSIONS: We concluded that IFI27, IFI44, IFITM3, FCER1A, and ISG15 may play a role in RSV. Our finding may contribute to the development of new potential biomarkers, reveal the underlying pathogenesis and also identify novel therapeutic targets for RSV. BioMed Central 2021-01-08 /pmc/articles/PMC7796524/ /pubmed/33419394 http://dx.doi.org/10.1186/s12887-020-02480-4 Text en © The Author(s) 2021 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Article Li, Lei Ni, Yong An Song, Zhenfeng Yi, Zhi Wang, Fang Identification of pathogenic genes and transcription factors in respiratory syncytial virus |
title | Identification of pathogenic genes and transcription factors in respiratory syncytial virus |
title_full | Identification of pathogenic genes and transcription factors in respiratory syncytial virus |
title_fullStr | Identification of pathogenic genes and transcription factors in respiratory syncytial virus |
title_full_unstemmed | Identification of pathogenic genes and transcription factors in respiratory syncytial virus |
title_short | Identification of pathogenic genes and transcription factors in respiratory syncytial virus |
title_sort | identification of pathogenic genes and transcription factors in respiratory syncytial virus |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7796524/ https://www.ncbi.nlm.nih.gov/pubmed/33419394 http://dx.doi.org/10.1186/s12887-020-02480-4 |
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