In contrast, DC-SIGNR cross-linkswith multiple glycan-nanoparticles, resulting in extended large-scalenanoparticle–lectin assemblies and markedly weaker affinitiescompared to DC-SIGN.14,20 Moreover, we have found thatthese glycan-nanoparticles only potently and robustly block DC-SIGN-,but not DC-SIGNR-, mediated augmentation of cell entry of Ebola glycoproteinpseudotyped viruses, thus demonstrating the critical role of the MLGIbinding mode of glycoconjugates in their ability to block cell surfacelectin receptor-mediated viral infections.14 The gene discussed is CLEC4M; the disease is viral infectious disease.