These data provide evidence of the biological relevance of DDX50 during infection, with the increased plaque formation efficiency on DDX50 KO cells correlating with an early defect in IRF3-dependent antiviral signalling, although we cannot rule out alternative mechanisms contributing to DDX50-dependent restriction, with many DExD/H-Box RNA helicases reported to restrict viral replication independently of any known role in antiviral signalling [20]. This evidence concerns the gene IRF3 and infection.