RVFV NSs protein is not essential for virus replication in cell cultures [19, 20] , yet plays a critical role in viral virulence [21] . A naturally occurring RVFV mutant Clone 13, which lacks approximately 70% of the NSs gene [20] , is highly attenuated in mouse, and, when reassortant viruses between wt RVFV and Clone 13 were characterized, the NSs was revealed as a major determinant of viral virulence in the mouse model [21] . The NSs localizes in the nucleus and cytoplasm in both RVFV-infected cells and NSs-expressing cells; further, the nuclear NSs, but not the cytoplasmic NSs, forms a unique filamentous structure [24] . The NSs suppresses the transcription of host mRNAs by interacting with the p44 subunit of TFIIH, an essential transcriptional factor for cellular RNA polymerase II [25] . Furthermore, the RVFV NSs binds to Sin3A-Associated Protein 30 (SAP30), which is important for maintaining the repressor complex containing histone deacetylase 3 on the interferon (IFN)-b promoter, and suppresses the IFN-b promoter activation early in infection [26] . Accordingly, the NSs protein in the nucleus of infected cells most probably exerts these host transcriptional-suppressive activities, including that of IFN production inhibition, and contributes to viral virulence [21] . In contrast, the biological function of cytoplasmic NSs is largely unknown. RVFV NSs expression promotes RVFV minigenome RNA synthesis driven by N and L protein in expression studies [27] . Because RNA synthesis of bunyaviruses occurs in the cytoplasm, NSs protein in cytoplasm may promote the minigenome RNA synthesis by unknown mechanism.