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2024-4-15 15:22:44

Le Y, Zhang J, Gong Z, Zhang Z, Nian X, Li X, Yu D. TRAF3 deficiency in MDCK cells improved sensitivity to the influenza A virus. Heliyon. 2023 Aug 21;9(9):e19246
submited by kickingbird at Sep, 10, 2023 9:2 AM from Heliyon. 2023 Aug 21;9(9):e19246

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.

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