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

在本研究中，我们旨在阐明SeV基质蛋白M诱导的宿主细胞骨架重组对病毒组装和萌发的重要性，我们发现SeV M蛋白能够以Rho家族GTPase CDC42依赖的方式诱导肌动蛋白细胞骨架重组形成丝状肌动蛋白结构。这种肌动蛋白重组对于单独表达M形成的病毒样颗粒的有效萌发是重要的。此外，我们还展示了一种病毒辅助蛋白C对病毒核糖核酸合成的极化调节机制，C蛋白在病毒复制中的潜在重要性，另一种病毒辅助蛋白V抑制干扰素-β诱导的新机制，以及病毒核蛋白N在限制DI基因组生产和逃避宿主固有免疫传感器检测病毒感染方面的重要性。

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.