Previously, a VSV replicon vector was generated by replacing the glycoprotein G gene of VSV with the hemagglutinin (HA) gene of an H7N1 influenza virus and inserting an extra transcription unit into the HA-L intergenic junction to drive expression of a modified GFP gene [28] . In the present work, this vector was modified by inserting the firefly luciferase gene into the transcription unit at position 5 (thereby replacing the GFP gene) and exchanging the HA gene with the GFP gene (Fig. 1a) . The resulting vector, VSV*DG(Luc), was propagated on BHK-G43 helper cells which express the VSV G protein in an inducible manner [23] . Up to 10 9 virus replicon particles (VRP) were released into the cell culture supernatant 24 h post infection (data not shown). Several mammalian and avian cells were found to be susceptible to infection with the VRPs in line with previous observations on the very broad cell tropism of VSV [29] . Infected cells were readily detected (5 to 6 h post infection) by means of GFP reporter expression (Fig. 1b) . However, non-helper cells were unable to complement the VSV G deletion and thus could not produce infectious progeny virus. Importantly, VSV*DG(Luc) did not induce type I IFN in the cell lines analysed (data not shown). This can be ascribed to the host shut-off activity of the VSV matrix protein [30] .