As shown in Fig. 1E, after infection with a defective interfering (DI) genome-rich Sendai virus (SeV) preparation, human 293T cells induced robust amounts of IFN-β promoter-driven FF-Luc activity when we transfected an empty vector or upon expression of a double mutant of NS1 from PR8 (PR8 R38A K41A) that was previously found to abrogate the RNA binding activity (49, 50). This evidence concerns the gene IFNB1 and infection.