Abstract
Infection of untransformed cells with a wide-range of non-oncogenic enveloped viruses causes a significant increase in their susceptibility to agglutination by concanavalin A (Con A). The increased Con A agglutinability of these cells is not caused by an increase in the number of Con A sites on the cell surface but involves alteration in the surface properties of infected cells to allow redistribution of Con A receptors to form "patches" following binding of Con A to the cell surface. Similarities between Con A-mediated agglutination of normal cells infected with non-oncogenic viruses and the agglutination response to cells transformed by oncogenic viruses will be reviewed. Finally, the use of Con A as an experimental tool to modify the replication and cytopathogenicity of non-oncogenic viruses grown in mammalian cells will be presented.
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