Extended Data Fig. 10: Overexpression of DSC2 mediated EBV epithelial entry is independent on EphA2, but EphA2 mediating EBV infection depended on DSC2/3. Related to Fig. 5.
From: Epstein–Barr virus exploits desmocollin 2 as the principal epithelial cell entry receptor
a, NOK cells overexpressing mCherry or DSC2-mCherry, along with control or EPHA2 CRISPR knockout, were infected with EBV through cell-cell contact or cell free EBV. The infection efficiency was determined by fluorescence microscope. b, EphA2-mcherry was expressed in control NOK cells or NOK single clone cells with DSC2/3 double knockout. Expression of DSC2, DSC3 or EphA2-mCherry was assessed by western blotting. c, Expression of mCherry, DSC2-mCherry or EphA2-mCherry in YCCEL1 cells, was analyzed by western blotting with mCherry antibody. GAPDH served as an internal control. d, Cartoon schematic summarizing the role of DSC2/3 as receptors for EBV epithelial infection via the cell-free and cell-cell routes of infection, created with BioRender.com. Experiments were performed twice (a, b) or thrice (c) with similar results. Scale bars, 150 μm. Panel d created with BioRender.com.
