We wanted to know if one of these viral proteins is able to block the transcription from the IFNb promoter in Vero cells infected with NDV. To address this question we co-transfected these viral protein expression constructs together with our reporter plasmids pIFNb-luc and pJATLacZ into Vero cells. Then the transfected cells were infected with NDV and luciferase activity in cell extracts was analysed ( fig. 5b ). Neither the nucleoprotein nor the glycoproteins could impede NDV-induced transcriptional upregulation of the IFNb promoter. All three amino-terminal expression constructs containing the OTU domain of the GV L protein (L1-169, L1-667 and L1-1757) were able to significantly decrease luciferase expression, whereas the C-terminal part of L (L1749-3391), which contains parts of the polymerase but no OTU domain, showed no effects on NDV-induced reporter gene expression. The protein L1-169 was more effective than L1-667 and L1-1757 in blocking NDV-induced IFNb-promoter activity. These data strongly suggest that the GV OTU domain is responsible for the inhibitory effects on type I interferon induction observed in infected cells (fig. 2 ).