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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,...

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Detalles Bibliográficos
Autores principales: 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
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2023
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
Descripción
Sumario: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.