The results revealed that the transcription levels of IFN-β, OAS2, RIG-I, ISG15, and IFI16 were significantly higher in VSV-Sp100A- and VSV-Sp100A-S188D-infected cells than in cells inoculated with VSV-GFP and that replacement of Sp100A with Sp100A-S188A in recombinant VSV remarkably reduced the protein’s capability to induce the above ISGs during virus infection (Fig. 4E and Fig. S3G). Here, RIGI is linked to viral infectious disease.