We wanted to know if NSDV is able to interfere with type I and type II IFN signalling. Vero cells were transfected with plasmids having the luciferase ORF under the control of the mouse Mx1 promoter (a promoter strongly activated by type I IFN) or one containing multiple copies of a GAS element (responds to type II IFN). Those cells were subsequently infected with either the GV or the NSDV isolate. After eighteen hours of infection cells were treated with IFNa or IFNc or left untreated. Finally the luciferase activity was determined as described in material and methods. Treatment of cells with IFNa induced high levels of luciferase activity in cells transfected with the Mx-1 reporter plasmid ( fig. 3a ) which is in accordance with the literature [38] . Infection with either GV or NSDV resulted in a significant reduction in IFNinduced Mx-1 promoter activity when compared to uninfected cells. The same effect could be observed when cells were treated with IFNc to induce the GAS element ( fig. 3b ). GV and NSDV were similarly effective in reducing the promoter activity in the presence of IFNc to less than forty percent of the activity in IFNcstimulated uninfected cells. These data strongly suggest that NSDV/GV is able to counteract the type I and II IFN induced transcription of genes that have an ISRE or GAS element in their promoters.