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TRAF3 deficiency in MDCK cells improved sensitivity to the influenza A virus
Tumor necrosis factor receptor-associated factor 3 (TRAF3), an adaptor protein, has significant and varying effects on immunity depending on cell types. The role of TRAF3 in Madin-Darby Canine Kidney Epithelial (MDCK) cell resistance to influenza A virus (IVA) remains elusive. In the present study,...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10481187/ https://www.ncbi.nlm.nih.gov/pubmed/37681145 http://dx.doi.org/10.1016/j.heliyon.2023.e19246 |
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author | Le, Yang Zhang, Jiayou Gong, Zheng Zhang, Zhegang Nian, Xuanxuan Li, Xuedan Yu, Daiguan Ma, Ning Zhou, Rong Zhang, Guomei Liu, Bo Yang, Lu Fu, Baiqi Xu, Xiuqin Yang, Xiaoming |
author_facet | Le, Yang Zhang, Jiayou Gong, Zheng Zhang, Zhegang Nian, Xuanxuan Li, Xuedan Yu, Daiguan Ma, Ning Zhou, Rong Zhang, Guomei Liu, Bo Yang, Lu Fu, Baiqi Xu, Xiuqin Yang, Xiaoming |
author_sort | Le, Yang |
collection | PubMed |
description | Tumor necrosis factor receptor-associated factor 3 (TRAF3), an adaptor protein, has significant and varying effects on immunity depending on cell types. The role of TRAF3 in Madin-Darby Canine Kidney Epithelial (MDCK) cell resistance to influenza A virus (IVA) remains elusive. In the present study, CRISPR-Cas9 gene editing technology was used to construct the TRAF3 knockout MDCK cells (MDCK-TRAF3(−/−)). Hemagglutination assay, plaque assay, transcriptome, and quantitative real-time PCR were performed after IVA infection. The results showed that after IVA infection, HA titers and virus titers were promoted, interferon I-related pathways were significantly blocked, and transcription of several antiviral-related genes was significantly decreased in MDCK-TRAF3(−/−) cells. Thus, our study suggests that TRAF3 gene knockout reduced MDCK cell's resistance to IVA, thereby resulting in a promising way for IVA isolation and vaccine manufacturing. |
format | Online Article Text |
id | pubmed-10481187 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-104811872023-09-07 TRAF3 deficiency in MDCK cells improved sensitivity to the influenza A virus Le, Yang Zhang, Jiayou Gong, Zheng Zhang, Zhegang Nian, Xuanxuan Li, Xuedan Yu, Daiguan Ma, Ning Zhou, Rong Zhang, Guomei Liu, Bo Yang, Lu Fu, Baiqi Xu, Xiuqin Yang, Xiaoming Heliyon Research Article Tumor necrosis factor receptor-associated factor 3 (TRAF3), an adaptor protein, has significant and varying effects on immunity depending on cell types. The role of TRAF3 in Madin-Darby Canine Kidney Epithelial (MDCK) cell resistance to influenza A virus (IVA) remains elusive. In the present study, CRISPR-Cas9 gene editing technology was used to construct the TRAF3 knockout MDCK cells (MDCK-TRAF3(−/−)). Hemagglutination assay, plaque assay, transcriptome, and quantitative real-time PCR were performed after IVA infection. The results showed that after IVA infection, HA titers and virus titers were promoted, interferon I-related pathways were significantly blocked, and transcription of several antiviral-related genes was significantly decreased in MDCK-TRAF3(−/−) cells. Thus, our study suggests that TRAF3 gene knockout reduced MDCK cell's resistance to IVA, thereby resulting in a promising way for IVA isolation and vaccine manufacturing. Elsevier 2023-08-21 /pmc/articles/PMC10481187/ /pubmed/37681145 http://dx.doi.org/10.1016/j.heliyon.2023.e19246 Text en © 2023 Published by Elsevier Ltd. 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 | Research Article Le, Yang Zhang, Jiayou Gong, Zheng Zhang, Zhegang Nian, Xuanxuan Li, Xuedan Yu, Daiguan Ma, Ning Zhou, Rong Zhang, Guomei Liu, Bo Yang, Lu Fu, Baiqi Xu, Xiuqin Yang, Xiaoming TRAF3 deficiency in MDCK cells improved sensitivity to the influenza A virus |
title | TRAF3 deficiency in MDCK cells improved sensitivity to the influenza A virus |
title_full | TRAF3 deficiency in MDCK cells improved sensitivity to the influenza A virus |
title_fullStr | TRAF3 deficiency in MDCK cells improved sensitivity to the influenza A virus |
title_full_unstemmed | TRAF3 deficiency in MDCK cells improved sensitivity to the influenza A virus |
title_short | TRAF3 deficiency in MDCK cells improved sensitivity to the influenza A virus |
title_sort | traf3 deficiency in mdck cells improved sensitivity to the influenza a virus |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10481187/ https://www.ncbi.nlm.nih.gov/pubmed/37681145 http://dx.doi.org/10.1016/j.heliyon.2023.e19246 |
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