Next we wanted to examine if the absence of IFNb promoter activation in early stages of NSDV infection upon NSDV/GV infection is due to an active block or if NSDV/GV is rather avoiding the activation of the IFNb promoter by a similar mechanism as already described for CCHFV [21] . On that account we transfected Vero cells with the IFNb reporter gene plasmid. One day later cells were infected with the GV or NSDV isolate, and subsequently super-infected with NDV. Immunofluorescence experiments showed that approx 85% of cells were infected with NSDV/GV, and that prior infection with NSDV/ GV did not block NDV infection in these cells (data not shown). The reporter gene activity was determined as described in material and methods ( fig. 2 ). In cells infected with NDV alone the expected increase in the activity of the IFNb promoter was observed when compared to uninfected cells. Interestingly, when the NDV infection was preceded by infection with GV or NSDV there was a clear reduction in the promoter activation detectable compared to cells infected solely with NDV. The reduction in the effects of NDV in these assays was only 40% even though about 85% of the cells were infected with NSDV/GV. This may have been because there was insufficient NSDV/GV protein at the time of the NDV superinfection to provide a complete block of the IFN induction pathway inside each infected cell; the reduction in reporter gene activity was indeed less pronounced if NDV was applied after shorter periods of GV or NSDV infection such as four hours post infection (data not shown), showing that it takes some time for the active block of the IFN induction pathway to take effect. This discrepancy may also reflect the limited nature of the block provided by NSDV/GV, which is unable to completely prevent activation of the IFN-beta promoter later in its own infection (FIg 1b) , as well as the very strong stimulus provided by the NDV superinfection in these experiments. Nevertheless, these results indicate that NSDV and GV are able to actively suppress activation of the IFNb promoter, and are not simply avoiding detection by cellular PRRs.