Viral recognition and entry depends on the affinity of the glycosylated envelope proteins to the host cells’ surface proteins.59 The spontaneous mutation and loss of oligosaccharide attachment sites prevent reading recognition of viral glycosylation of viral envelope glycoproteins.60 Continued challenges are there to enable broad-spectrum viral suppression support lectins as inhibitors of viral entry in the provision of prophylactic and potential viral infection therapeutics.61 The envelope proteins have a shared tertiary and quaternary architecture and function similarly. The gene discussed is ERVW-1; the disease is viral infectious disease.