Fig. 5: FCHO1 deficiency does not alter global clathrin-mediated endocytosis.

a, b Fusion of VSV-G HIV-1ΔEnv (BlaM-Vpr) virions (a) or infection by VSV-G HIV-1ΔEnv (b) of Jurkat cells. Wt or FCHO1-deficient clones were challenged with increasing volumes of the indicated VSV-G HIV-1ΔEnv. Virion fusion was monitored by flow cytometry as previously reported^29,30,31 and the percentage of cleaved CCF2⁺/BlaM-Vpr⁺ cells is plotted relative to the virus inoculum. Infection of VSV-G HIV-1ΔEnv was monitored by intracellular HIV-1 p24 staining two days post challenge and the relative percentage of p24-positive cells is plotted relative to the virus inoculum³². Arithmetic means and standard errors are shown of results obtained for the indicated number of clones from either virion fusion (e) or infection (f). c Patient fibroblast or healthy donor fibroblast were subjected to the transferrin uptake assay. Cells were exposed to fluorescently labelled transferrin for the indicated time at 37 °C and subsequently analysed by FACS. Data are pooled of four independent assays; error bars represent standard deviation. a–c Statistical analysis was performed using two-way ANOVA (p-values for the effect of the genotype). Source data are provided as a Source Data file.