Next, we tested if partial deletions within the NSs gene would affect the inhibition of IFN-b mRNA synthesis. Type-I IFNcompetent A549 cells were mock-infected or infected with MP-12, rMP12-C13type or NSs mutants at an moi of 3, and then total RNA was extracted at 7 hpi. Northern blot was performed using RNA probe specific to human IFN-b, ISG56 or RVFV anti-viralsense S RNA/N mRNA as described previously [66, 67] . We tested ISG56 gene, one of the genes controlled under IFN-stimulated response element (ISRE), to confirm the inhibition of host transcription suppression including IFN-b mRNA by NSs. As expected, cells infected with MP-12 inhibited the synthesis of IFNb and ISG56 mRNA, while those infected with rMP12-C13type induced both IFN-b and ISG56 mRNA (Fig. 2B) . Interestingly, none of NSs mutants, including NSD210-230 lacking SAP30binding domain, had inhibited IFN-b mRNA synthesis. Viral replication of those mutants was significantly decreased in type-I IFN-competent MRC-5 cells (Fig. S2) . Therefore, it was concluded that a series of MP-12 encoding partially truncated NSs gene does not degrade PKR and inhibit IFN-b mRNA synthesis.