Fig. 2: IDH1 mutation enhances VSVΔ51 replication in glioma.

a Cells were pretreated with or without doxycycline (DOX) for 48 h, followed by VSVΔ51–GFP infection (MOI = 0.01 for LN-229, MOI = 0.1 for LN-18) for the indicated times. Phase-contrast and fluorescence microscopy images were captured. Representative images of n = 3. b Green fluorescent signals were measured, counted and analyzed in cells treated as in a. n = 4 biological replicates. c Relative cell growth rate was measured in cells treated as in a. n = 4 biological replicates. d Cells were infected with VSVΔ51 (MOI = 0.01 for LN-229, MOI = 0.1 for LN-18) for 24 h in the presence or absence of DOX, viral protein VSV-G was analyzed by western blot. e Cells were infected with VSVΔ51 (MOI = 0.01 for LN-229, MOI = 0.1 for LN-18) for the indicated times in the presence or absence of DOX, single-step growth analyses were conducted. n = 3 biological replicates. f–i Cells were infected with VSVΔ51 (MOI = 0.01 for GBM02, MOI = 1 for GL261) for 24 h in the presence or absence of DOX. f, h Viral protein VSV-G was analyzed by western blot. g, i Corresponding viral titers in supernatants were determined. n = 3 biological replicates. j–l The bilaterally implanted mice were treated with VSVΔ51 (3 × 10⁷ PFU) by intravenous injection, and tumors were resected at 24 h after injection. j Schematic illustration of the bilaterally subcutaneous transplantation model. k Immunofluorescence staining was used to evaluate the expression of GFP (reporter gene for VSVΔ51) and Flag-IDH1(R132H). Representative images of n = 3. l Subcutaneous tumor titers are shown for animals sacrificed 24 h after virus administration. n = 5 mice per group. Statistical significance was determined using two-way ANOVA in c, or two-tailed Student’s t-test in e, g, i, l. Data represent the mean ± SD. Scale bar, 50 μm. Source data are provided in the Source Data file.