Elucidation of mechanism for reorganization of host cytoskeletoninduced by Sendai virus matrix protein

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In this study, we aimed at elucidation of importance of reorganization of host cellular cytoskeleton induced by SeV matrix protein M on viral assembly and budding, and we found that SeV M protein has the ability to induce reorganization of actin cytoskeleton to form filopodia-like actin-based structure in a Rho-family GTPase Cdc42-dependent manner. This actin reorganization was important for efficient budding of virus-like particles formed by expression of M alone. In addition, we also showed a mechanism for polarized regulation of viral RNA synthesis by one of the SeV accessory protein C, a potential importance of C protein on viral replication, a novel mechanism for inhibition of IFN-β induction by another SeV accessory protein V, and an importance of SeV nucleoprotein N on restriction of DI genome produc tion and evasion form detection of viral infection by host innate immune sensors.