The cell-rounding activity of the vesicular stomatitis virus matrix protein is due to the induction of cell death.

Abstract

The matrix (M) protein of vesicular stomatitis virus (VSV) expressed in the absence of other viral components causes many of the cytopathic effects of VSV, including an inhibition of host gene expression and the induction of cell rounding. It was recently shown that M protein also induces apoptosis in the absence of other viral components. This raises the possibility that the activation of apoptotic pathways causes the inhibition of host gene expression and cell rounding by M protein. To test this hypothesis, host gene expression and cell rounding were analyzed after the transfection of M mRNA into HeLa cells stably overexpressing Bcl-2 (HeLa-Bcl-2 cells). We have shown previously that Bcl-2 inhibits M-protein-induced apoptosis. Here, we show that activation of the apoptotic pathways downstream of Bcl-2 is not required for the inhibition of host gene expression by M protein. In contrast, overexpression of Bcl-2 inhibited cell rounding induced by M protein, indicating that apoptotic pathways downstream of Bcl-2 are required for the cell-rounding activities of M protein.