In an initial experiment we wanted to determine whether CHO-K1 cells are susceptible to VSVDG/LASVGP infection. The reason we chose CHO-K1 cells for our studies is the availability of a site 1 protease-deficient CHO cell line (designated SRD-12B cells), in which GP maturation is abolished and only GP-deficient non-infectious LASV particles are released [23] . Thus, this cell clone provides an ideal control for inhibition studies. Vero E6, CHO-K1, and SRD-12B cells were infected with either VSVDG/ LASVGP or wild-type VSV (VSVwt) as a control. Aliquots of cell culture supernatants were collected at different times after infection and were analyzed by plaque assay. Growth kinetics revealed that VSVDG/LASVGP grows to similar titers in CHO-K1 cells compared to Vero E6 cells which have been used in earlier studies (Fig. 1A) [48] . These data demonstrated that CHO-K1 cells support efficient VSVDG/LASVGP replication, and thus are useful tools for further investigations. As expected, VSVDG/ LASVGP lacks efficient replication in SRD-12B cells, whereas virus growth of VSVwt remained unaffected in these cells (Fig. 1A) . The reason for the low but detectable virus titers in the supernatant of VSVDG/LASVGP-infected SRD-12B cells is currently not known but has been also observed for LASV ( [23] and present study), LCMV [34] and New Word arenaviruses [33] . Glycoprotein activation by a yet unknown protease though with only very low efficiency might explain this phenomenon.