To understand how the NSs protein exerted an efficient viral replication in the presence of ActD, we analyzed the status of host and viral translation. VeroE6 cells were mock-infected or independently infected with MP-12, rMP12-rLuc and rMP12-C13type, the latter of which lacks approximately 70% of the NSs ORF ( Figure 1A) , at an moi of 3. Cells were radiolabelled with [ 35 S] Methionine/Cysteine from 15 to 16 h.p.i. Cell extracts were prepared at 16 h.p.i., and the samples were applied to SDS-PAGE ( Figure 1C , top panel). In the absence of ActD, the host protein synthesis of rMP12-rLuc-infected cells ( Figure 1C , lane 5) and rMP12-C13type-infected cells ( Figure 1C , lane 7) was more efficient than that of MP-12-infected cells ( Figure 1C , lane 3). It is possible that NSs-mediated transcriptional suppression that occurred only in MP-12-infected cells, but not in cells infected with viruses lacking NSs, caused a reduction of host mRNA abundance, leading to the less efficient translation of host mRNAs in MP-12-infected cells. Efficient N protein synthesis occurred in cells infected with all three viruses in the absence of ActD, a finding which was consistent with our previous studies [19] , while for some unknown reasons the accumulation of N proteins of rMP12-rLuc and rMP12-C13type was slightly higher than that of MP-12. ActD treatment resulted in a strong inhibition of both host proteins and N protein synthesis in rMP12-rLuc-infected cells ( Figure 1C , lane 6) and rMP12-C13type-infected cells ( Figure 1C , lane 8). In contrast, ActD treatment did not inhibit N protein translation in MP-12-infected cells; rather, it moderately inhibited host protein synthesis in MP-12-infected cells ( Figure 1C, lane 4) . A similar ActD-induced, moderate host protein synthesis inhibi-