| Abstract |
Low-neurovirulence BeAn and DA Theiler's murine encephalomyelitis viruses (TMEV) cause persistent infection in the central nervous system (CNS) of susceptible mouse strains, leading to an inflammatory demyelinating process. A role for a specific virus-cell receptor interaction has been posited to explain why only low- and not high-neurovirulence TMEV cause persistent CNS infections. Low- but not high-neurovirulence TMEV use sialic acid for attachment to mammalian cells, which may contribute to neurovirulence attenuation and viral persistence. Analysis of BeAn virus binding and infection in cells with altered (mutated) cell-surface expression of sialic acid containing glyconjugates indicated that both binding and infection are mediated entirely by N-linked glycoproteins. By contrast, GDVII virus binding and infection appears to be dependent only in part on N-linked glycoproteins and not on O-linked glycoproteins or glycolipids. These results indicate that low-neurovirulence BeAn virus uses a sialic acid moiety expressed on an N-linked carbohydrate of a glycoprotein that serves as the protein entry receptor.
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