Rotavirus infection is the most significant cause of gastroenteritis in the young [1], leading to death of approximately 440,000 children annually, worldwide [2].The tremendous incidence of rotavirus infection and associated economic burden underscores the urgent need for the development of a therapeutic.Rotaviruses infect only the mature enterocytes on intestinal villi, suggesting the existence of a specific host cell receptor [3].Binding and penetration of the virion is a complex process with multiple cell surface interactions, some being speciesspecific [4].It is accepted that rotavirus virions bind to glycoconjugates on the host cell surface, however their critical chemical components are not defined, and the relevance of involvement of sialic acids is controversial [5].Host-cell attachment occurs via the outer capsid spike protein VP4, after tryptic cleavage that produces an N-terminal fragment,VP8*.A structure of VP8* bound to a sialic acid has been determined by X-ray crystallography [6].