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Global transcriptome analysis of H5N1 influenza virus-infected human cells
BACKGROUND: Influenza A virus (IAV) belongs to the Orthomyxoviridae family. IAV causes a highly contagious respiratory disease in humans that exacts severe economic losses globally. The virus uses strategies developed to exploit and subvert cellular proteins and pathways to increase its own replicat...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6366111/ https://www.ncbi.nlm.nih.gov/pubmed/30774581 http://dx.doi.org/10.1186/s41065-019-0085-9 |
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author | Cao, Ying Zhang, Kun Liu, Lirong Li, Wei Zhu, Bin Zhang, Shuang Xu, Ping Liu, Wenjun Li, Jing |
author_facet | Cao, Ying Zhang, Kun Liu, Lirong Li, Wei Zhu, Bin Zhang, Shuang Xu, Ping Liu, Wenjun Li, Jing |
author_sort | Cao, Ying |
collection | PubMed |
description | BACKGROUND: Influenza A virus (IAV) belongs to the Orthomyxoviridae family. IAV causes a highly contagious respiratory disease in humans that exacts severe economic losses globally. The virus uses strategies developed to exploit and subvert cellular proteins and pathways to increase its own replication and to inhibit antiviral immune response. RESULTS: A/bar-headed goose/Qinghai/1/2005 (A/QH) was able to infect A549 and 293 T cells, with a high infection rate for A549 cells. To identify host cellular responses of human cells to influenza infection, differentially expressed genes (DEGs) between AIV-infected groups and uninfected controls were identified using RNA-sequencing. The DEGs were annotated by Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes pathway analyses, which revealed that the DEGs were mainly linked to cellular function and metabolic processes, while the cellular function that is probably associated with host cellular response of human cells, including defense response to virus and protein modification. All the DEGs and pathways were possibly involved in the response to IAV invasion. CONCLUSIONS: The global transcriptome analysis results revealed that sensitive genes and pathways of the cells were infected with the influenza virus and provided further evidence to investigate the complicated relationship between IAV and host cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s41065-019-0085-9) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-6366111 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-63661112019-02-15 Global transcriptome analysis of H5N1 influenza virus-infected human cells Cao, Ying Zhang, Kun Liu, Lirong Li, Wei Zhu, Bin Zhang, Shuang Xu, Ping Liu, Wenjun Li, Jing Hereditas Research BACKGROUND: Influenza A virus (IAV) belongs to the Orthomyxoviridae family. IAV causes a highly contagious respiratory disease in humans that exacts severe economic losses globally. The virus uses strategies developed to exploit and subvert cellular proteins and pathways to increase its own replication and to inhibit antiviral immune response. RESULTS: A/bar-headed goose/Qinghai/1/2005 (A/QH) was able to infect A549 and 293 T cells, with a high infection rate for A549 cells. To identify host cellular responses of human cells to influenza infection, differentially expressed genes (DEGs) between AIV-infected groups and uninfected controls were identified using RNA-sequencing. The DEGs were annotated by Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes pathway analyses, which revealed that the DEGs were mainly linked to cellular function and metabolic processes, while the cellular function that is probably associated with host cellular response of human cells, including defense response to virus and protein modification. All the DEGs and pathways were possibly involved in the response to IAV invasion. CONCLUSIONS: The global transcriptome analysis results revealed that sensitive genes and pathways of the cells were infected with the influenza virus and provided further evidence to investigate the complicated relationship between IAV and host cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s41065-019-0085-9) contains supplementary material, which is available to authorized users. BioMed Central 2019-02-06 /pmc/articles/PMC6366111/ /pubmed/30774581 http://dx.doi.org/10.1186/s41065-019-0085-9 Text en © The Author(s) 2019 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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. |
spellingShingle | Research Cao, Ying Zhang, Kun Liu, Lirong Li, Wei Zhu, Bin Zhang, Shuang Xu, Ping Liu, Wenjun Li, Jing Global transcriptome analysis of H5N1 influenza virus-infected human cells |
title | Global transcriptome analysis of H5N1 influenza virus-infected human cells |
title_full | Global transcriptome analysis of H5N1 influenza virus-infected human cells |
title_fullStr | Global transcriptome analysis of H5N1 influenza virus-infected human cells |
title_full_unstemmed | Global transcriptome analysis of H5N1 influenza virus-infected human cells |
title_short | Global transcriptome analysis of H5N1 influenza virus-infected human cells |
title_sort | global transcriptome analysis of h5n1 influenza virus-infected human cells |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6366111/ https://www.ncbi.nlm.nih.gov/pubmed/30774581 http://dx.doi.org/10.1186/s41065-019-0085-9 |
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