TRAF3 deficiency in MDCK cells improved sensitivity to the influenza A virus

Tumor necrosis factor receptor-associated 3 (TRAF3), an adaptor protein, has significant and varying effects on immunity depending cell types. The role of TRAF3 in Madin-Darby Canine Kidney Epithelial (MDCK) resistance to influenza A virus (IVA) remains elusive. In the present study, CRISPR-Cas9 gene editing technology was used construct knockout MDCK cells (MDCK-TRAF3−/−). Hemagglutination assay, plaque transcriptome, quantitative real-time PCR were performed after IVA infection. results showed that infection, HA titers promoted, interferon I-related pathways significantly blocked, transcription several antiviral-related genes decreased MDCK-TRAF3−/− cells. Thus, our study suggests reduced cell's IVA, thereby resulting a promising way for isolation vaccine manufacturing.