The mosquito-borne bunyavirus Rift Valley fever virus (RVFV) devastates both humans and domestic animals; it causes abortions in ruminants and complications such as hemorrhage, encephalitis, or retinal vasculitis in humans. A major RVFV virulence factor, NSs, disables host cell mRNA synthesis. Here we describe our new evidence that showed NSs working in a second way; in addition to inhibiting host cell transcription, NSs kept translation active in infected cells. It is well-established that activated protein kinase PKR phosphorylates a translation factor, eIF2a, and then this phosphorylated eIF2a suppresses translation. We found that NSs decreased PKR abundance and prevented eIF2a phosphorylation in infected cells, allowing efficient viral translation and replication. In contrast, when cells were infected with an RVFV mutant lacking NSs in the presence of transcriptional inhibitors that mimic the transcription inhibition function of NSs, the PKR reduction did not occur and phoshorylated eIF2a was accumulated, resulting in the inhibition of virus gene expression and replication. Thus, NSs functions in two ways to help RVFV replicate in mammalian hosts: its newly identified PKR downregulation function secures efficient viral translation, and its host transcription inhibition function suppresses the expression of host innate antiviral functions.