Extended Data Fig. 6: IGF1R expression in mosquito and human cells confers infectivity and binding to RSV.

a, Foci of RSV infection in 1HAEo⁻ cells pre-treated with inhibitors of cell-surface receptors. The results for treatment with inhibitors of other receptors are presented in Figs. 1e, 2a. **P < 0.01, ***P < 0.001 by one-way ANOVA and Tukey’s post hoc analysis. Data shown are the mean of n = 4 biological replicates and are representative of at least 2 independent experiments. b, RSV was incubated with 1HAEo⁻ cells for 60 min on ice and imaged by confocal microscopy. Arrowheads indicate the colocalization of RSV particles and IGF1R. Data shown are representative of multiple images of 3 independent repeats. c, Example flow cytometry plots of RSV–GFP-infected C636 mosquito cells transfected with human IGF1R. d, Plot summarizing the data from the flow cytometry experiments shown in c, indicating the percentage of cells infected by RSV. Bars indicate the mean of n = 3 biological replicates that are representative of 2 independent repeats; ***P < 0.001 by one-way ANOVA, with Tukey’s post hoc analysis. e, Western blot of IGF1R expression in wild-type 1HAEo⁻ cells and IGF1R knockout 1HAEo⁻ cells that were gene-edited using CRISPR–Cas9. IGF1R expression was rescued in knockout cells using lentiviral transduction (KO + IGF1R). Data is representative of 2 independent repeats. f, RSV-F^DS-Cav1 was bound to 1HAEo⁻ cells or IGF1R knockout cells on ice, then stained with a fluorescent antibody and quantified by a plate reader. Bars represent the mean of n = 5–7 biological replicates, representative of 2 independent repeats; *P < 0.05 by one-way ANOVA, Tukey’s post hoc analysis.