In contrast to members of the orthomyxovirus family, paramyxovirus replication takes place in the cytosol and, thus, is considered not to be immediately dependent on active cell proliferation [1] . In fact, MeV itself has been shown to induce a G 1 /S arrest in infected T lymphoyctes [29, 30] , confirming that cell cycle progression is not required for virus replication. To directly test whether the JMN3-003-mediated growth arrest per se is causal for the antiviral effect of the compound, we generated MeV-Alaska inhibition curves of JMN3-003 in comparison with the cyclin-dependent kinase inhibitor alsterpaullone. Even at the highest concentration assessed (50 mM), alsterpaullone caused only a marginal reduction in MeV yields (figure 4D). These findings indicate that the antiviral effect of JMN3-003 is based on an upstream effect of the compound rather than being a consequence of the cell cycle arrest itself. Cellular mRNA production and protein biosynthesis are unperturbed by JMN3-003