As inflammation and viral infection can stimulate production of galectins by endothelial cells [15], [16], [18], endogenous galectin-1 may contribute to host defense against NiV infection by mitigating the endothelial cell syncytia formation that is a hallmark of Nipah infection, as we have clearly demonstrated that endogenous galectin-1 can attenuate endothelial cell fusion in vitro (Fig. 2). This evidence concerns the gene LGALS1 and viral infectious disease.