RVFV has a single-stranded, tripartite RNA genome composed of the L, M, and S segments. The L segment is of negative polarity encoding the RNA-dependent RNA polymerase (L). The anti-viralsense M segment encodes two envelope glycoproteins, Gn and Gc, and two accessory proteins,14-kDa NSm that suppresses virusinduced apoptosis [8] and the 78-kDa protein. The S segment uses an ambisense strategy for gene expression; a nonstructural protein, NSs, is translated from viral-sense mRNA, while N protein is expressed from anti-viral-sense mRNA [1] . N protein and L protein are essential for viral RNA synthesis [1] and NSs protein suppresses host innate immune functions by suppressing host gene expression [9] , including interferon-b [10] , and promoting PKR degradation [11, 12] . Experiments using reassortant viruses between an attenuated MP-12 strain of RVFV and wild-type (wt) RVFV suggested that RVFV virulence characteristics in the mouse are under polygenic control [13] . Further studies using reassortant viruses between the wt ZH548 strain of RVFV and an attenuated RVFV isolate clone 13, a plaque clone variant of the wt 74HB59 strain carrying a deletion of 69% of the NSs gene [14] , suggested that RVFV mouse virulence is controlled by the S segment [15] . The importance of NSs on viral virulence was confirmed by using a wt RVFV lacking the entire NSs gene [16, 17] . Studies using the wt RVFV lacking the NSm gene showed that NSm also affected virus virulence in rats [18] . In contrast, how Gn and Gc envelope proteins and L protein contribute to viral virulence is unknown.