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Suppression of Rac1 Signaling by Influenza A Virus NS1 Facilitates Viral Replication
Influenza A virus (IAV) is a major human pathogen with the potential to become pandemic. IAV contains only eight RNA segments; thus, the virus must fully exploit the host cellular machinery to facilitate its own replication. In an effort to comprehensively characterize the host machinery taken over...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5116764/ https://www.ncbi.nlm.nih.gov/pubmed/27869202 http://dx.doi.org/10.1038/srep35041 |
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author | Jiang, Wei Sheng, Chunjie Gu, Xiuling Liu, Dong Yao, Chen Gao, Shijuan Chen, Shuai Huang, Yinghui Huang, Wenlin Fang, Min |
author_facet | Jiang, Wei Sheng, Chunjie Gu, Xiuling Liu, Dong Yao, Chen Gao, Shijuan Chen, Shuai Huang, Yinghui Huang, Wenlin Fang, Min |
author_sort | Jiang, Wei |
collection | PubMed |
description | Influenza A virus (IAV) is a major human pathogen with the potential to become pandemic. IAV contains only eight RNA segments; thus, the virus must fully exploit the host cellular machinery to facilitate its own replication. In an effort to comprehensively characterize the host machinery taken over by IAV in mammalian cells, we generated stable A549 cell lines with over-expression of the viral non-structural protein (NS1) to investigate the potential host factors that might be modulated by the NS1 protein. We found that the viral NS1 protein directly interacted with cellular Rac1 and facilitated viral replication. Further research revealed that NS1 down-regulated Rac1 activity via post-translational modifications. Therefore, our results demonstrated that IAV blocked Rac1-mediated host cell signal transduction through the NS1 protein to facilitate its own replication. Our findings provide a novel insight into the mechanism of IAV replication and indicate new avenues for the development of potential therapeutic targets. |
format | Online Article Text |
id | pubmed-5116764 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-51167642016-11-28 Suppression of Rac1 Signaling by Influenza A Virus NS1 Facilitates Viral Replication Jiang, Wei Sheng, Chunjie Gu, Xiuling Liu, Dong Yao, Chen Gao, Shijuan Chen, Shuai Huang, Yinghui Huang, Wenlin Fang, Min Sci Rep Article Influenza A virus (IAV) is a major human pathogen with the potential to become pandemic. IAV contains only eight RNA segments; thus, the virus must fully exploit the host cellular machinery to facilitate its own replication. In an effort to comprehensively characterize the host machinery taken over by IAV in mammalian cells, we generated stable A549 cell lines with over-expression of the viral non-structural protein (NS1) to investigate the potential host factors that might be modulated by the NS1 protein. We found that the viral NS1 protein directly interacted with cellular Rac1 and facilitated viral replication. Further research revealed that NS1 down-regulated Rac1 activity via post-translational modifications. Therefore, our results demonstrated that IAV blocked Rac1-mediated host cell signal transduction through the NS1 protein to facilitate its own replication. Our findings provide a novel insight into the mechanism of IAV replication and indicate new avenues for the development of potential therapeutic targets. Nature Publishing Group 2016-11-21 /pmc/articles/PMC5116764/ /pubmed/27869202 http://dx.doi.org/10.1038/srep35041 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Jiang, Wei Sheng, Chunjie Gu, Xiuling Liu, Dong Yao, Chen Gao, Shijuan Chen, Shuai Huang, Yinghui Huang, Wenlin Fang, Min Suppression of Rac1 Signaling by Influenza A Virus NS1 Facilitates Viral Replication |
title | Suppression of Rac1 Signaling by Influenza A Virus NS1 Facilitates Viral Replication |
title_full | Suppression of Rac1 Signaling by Influenza A Virus NS1 Facilitates Viral Replication |
title_fullStr | Suppression of Rac1 Signaling by Influenza A Virus NS1 Facilitates Viral Replication |
title_full_unstemmed | Suppression of Rac1 Signaling by Influenza A Virus NS1 Facilitates Viral Replication |
title_short | Suppression of Rac1 Signaling by Influenza A Virus NS1 Facilitates Viral Replication |
title_sort | suppression of rac1 signaling by influenza a virus ns1 facilitates viral replication |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5116764/ https://www.ncbi.nlm.nih.gov/pubmed/27869202 http://dx.doi.org/10.1038/srep35041 |
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