Activity of vesicular stomatitis virus M protein mutants in cell rounding is correlated with the ability to inhibit host gene expression and is not correlated with virus assembly function.

摘要

Wild-type (wt) matrix (M) protein of vesicular stomatitis virus (VSV) and mutant M proteins tsO82 and MN1 were compared for cell rounding induction. The ability to induce cell rounding was not correlated with the virus assembly function of tsO82 andMN1, but was correlated with the ability to inhibit host gene expression. Cell rounding induced by mutant proteins occurred at a slower rate than the wt M protein, and this suggested that some cytopathic activity was still maintained by the tsO82 protein. The MN1 protein which was non-functional in virus assembly, was nearly as effective as wt M protein in the induction of cell rounding. It is concluded that cell rounding results from the depolymerization and inhibition of microtubules.