To test the possibility that ActD treatment alone suppressed translation and RVFV NSs counteracted it, 293 cells were mocktreated or treated with 5 mg/ml of ActD. We examined the resulting polysome profiles at 16 h post-ActD treatment ( Figure  S1A ). Because ActD treatment at 5 mg/ml inhibits the transcription mediated by RNA polymerases I, II and III [28] , we expected a reduction in the abundance of cellular mRNAs, tRNAs, and ribosomal RNAs, leading to reduced abundances of polysomes. ActD treatment indeed resulted in a reduced abundance of polysomes, whereas it did not substantially alter the polysome pattern, a finding which suggested to us that ActD treatment did not abolish translational activities. To test the translational competence of the cells treated with transcriptional inhibitors, we transfected 293 cells with in vitro-synthesized RNA transcripts encoding rLuc gene. Cells were mock-treated or treated with ActD or a-amanitin, an RNA polymerase II inhibitor [29] . The rLuc activities at 16 h post-transfection were slightly increased in the cells treated with ActD or a-amanitin ( Figure S1B ), demonstrating active host translation activities in the presence of either ActD or a-amanitin. These data led to the suggestion that by combining the replication of RVFV lacking the NSs and treatment of ActD, a cellular condition that is unfavorable for translation could be induced and that NSs expression somehow altered the cellular environment from one that was translationally inactive to one translationally active.