Our previous experiments have shown that NSDV is able to inhibit the action of type I and type II IFNs in infected cells ( fig. 3) . To identify the viral protein that is responsible for this effect we transfected Vero cells with reporter plasmids carrying a luciferase gene under the control of type I and II IFN-responsive promoters (pGL3-Mx-1-luc and GAS-luc) together with the viral protein expression plasmids. The cells were treated with IFNa or IFNc to induce transcription from the IFN-responsive promoters and the luciferase induced was measured ( fig. 6 ). The reporter gene activity in cells treated with IFNa or IFNc was significantly reduced in the presence of the GV L protein constructs containing the OTU domain (L1-169, L1-667 and L1-1757) compared to cells transfected with empty plasmid only, whereas in cells expressing the nucleoprotein, the glycoproteins or the carboxy-terminal part of the L protein, treatment with IFNa or IFNc induced comparable levels of reporter gene activity to that found in cells expressing no viral protein. As in the studies of IFN induction, the two shortest versions of the GV L protein were the most efficient in blocking the action of IFNa and IFNc.