Endothelial Galectin-1 Binds to Specific Glycans on Nipah Virus Fusion Protein and Inhibits Maturation, Mobility, and Function to Block Syncytia Formation
Figure 2
Endogenous endothelial galectin-1 inhibits NiV-F and NiV-G mediated syncytia formation.
A, Activated HUVECs have increased cell surface galectin-1 compared to resting cells. Flow cytometric analysis of cell surface galectin-1 on resting (light grey) and activated (dark grey) HUVECs, and on resting HUVECs plus exogenous galectin-1 (black) Data are mean ± SEM of three independent experiments, each done in triplicate. B, Activated HUVECs are resistant to NiV-F and NiV-G mediated cell fusion. Heterologous cell fusion of resting (light grey) and activated (dark grey) HUVECs, and resting HUVECs plus exogenous galectin-1 (black). Data are mean ± SD of triplicate samples from one of three replicate experiments. C, Reduction of cell surface galectin-1 by siRNA. Flow cytometric analysis of cell surface galectin-1 on resting HUVECs (grey filled), siRNA treated HUVECs (grey line), and siRNA treated HUVECS with 20µM exogenous galectin-1 (black line). D, Reduction of cell surface galectin-1 in HUVECs increases susceptibility to NiV-F and G mediated cell fusion. Heterologous cell fusion of resting cells (light grey), cells with reduced galectin-1 (white), and cells with reduced galectin-1 plus exogenous galectin-1 (dark grey). Data are mean ± SD of triplicate samples from one of three replicate experiments.