Skip to main content
. Author manuscript; available in PMC: 2016 Mar 18.
Published in final edited form as: Science. 2005 Apr 14;308(5728):1643–1645. doi: 10.1126/science.1110656

Fig. 1.

Fig. 1

Endosomal cysteine proteases CatB and CatL are host factors for VSV-GPΔMuc infection. (A and B) (Top) Effect of CatB-selective inhibitor CA074 (A) and CatL/CatB inhibitor FYdmk (B) on infectivities of VSV-G and VSV-GPΔMuc in Vero cells. (Bottom) CatB (A) and CatL (B) enzymatic activities in CA074- and FYdmk-treated Vero cells. Infectivities [infectious units (iu)/ml] are relative to the infectivity of the same virus in dimethyl sulfoxide (DMSO)–treated Vero cells (set to 100%) (25). (C) Wild-type (WT) and CatB-deficient (CatB−/− CatL+/+) MEFs were not transfected (none) or transfected with plasmid DNAs encoding β-galactosidase (β-gal), CatB (CatB), or CatL (CatL). After 24 hours, cells were exposed to VSV-GPΔMuc (~1 iu per cell), and the percentage of infected cells was determined 24 hours later by flow cytometry (25). (D) Capacity of VSV-GPΔMuc to infect CatB/CatL-deficient (CatB−/−CatL−/−) MEFs was determined as in (C). Infectivities from two replicates are shown in (A) and (B) and are representative of four independent experiments. Error bars, SD from at least three replicates.