Ganglioside GMia on the Cell Surface Is Involved in the Infection by Human Rotavirus KUN and MO Strains

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Abstract
Rotavirus is the most common cause of severe gastroenteritis in infants and children worldwide. The cell attachment of most animal rota viruses, which belong to the neuramin-idase-sensitive strains, requires sialic acid residues on the host cell membranes. On the other hand, most human rotaviruses are classified as neuraminidase-insensitive strains. The involvement of gangliosides on the host cell surface in human rotavirus infection was investigated by immunostaining analysis of target cells, and by assaying the neutralization of infection by rotavirus and the blocking of target cellular receptors. In host cells (MA104 cells) pretreated with Arthrobacter ureafaciens neuraminidase, which were still infected by human rotaviruses (KUN and MO strains), GM3 was hydrolyzed markedly by the neuraminidase, while GM1B was not hydrolyzed at all. Infection by the rotaviruses was strongly inhibited by exogenous ganglioside GM10, but not GA, Infection was also inhibited by pretreatment of the MA104 cells with cholera toxin B-subunit, which specifically blocked ganglioside GMla on the plasma membrane. The treatment of MA104 cells with the endoglycoceramidase attenuated human rotavirus infection. From these findings, we concluded that GM1a on the plasma membrane of the host cells was involved in the infection by human rotavirus KUN and MO strains.

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