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首页> 外文期刊>Journal of Virology >Maturation of viral proteins in cells infected with temperature-sensitive mutants of vesicular stomatitis virus.
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Maturation of viral proteins in cells infected with temperature-sensitive mutants of vesicular stomatitis virus.

机译：病毒蛋白在感染的细胞中感染的细胞敏感性突变体的脉湿性静脉炎病毒。

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Maturation of viral proteins in cells infected with mutants of vesicular stomatitis virus was studied by surface iodination and cell fractionation. The movement of G, M, and N proteins to the virion bud appeared to be interdependent. Mutations thought to be in G protein prevented its migration to the cell surface, allowed neither M nor N protein to become membrane bound, and blocked formation of viral particles. Mutant G protein appeared not to leave the endoplasmic reticulum at the nonpermissive temperature, but this defect was partially reversible. In cells infected with mutants that caused N protein to be degraded rapidly or prevented its assembly into nucleocapsids, M protein did not bind to membranes and G protein matured to the cell surface, but never entered structures with the density of virions. Mutations causing M protein to be degraded prevented virion formation, and G protein behaved as in cells infected by mutants in N protein. These results are consistent with a model of virion formation involving coalescence of soluble nucleocapsid and soluble M protein with G protein already in the plasma membrane.
机译：通过表面碘化和细胞分级研究了用囊泡口炎病毒突变体感染的病毒蛋白的成熟。 G，M和N蛋白的运动似乎是相互依赖的。被认为是在G蛋白中的突变阻止其迁移到细胞表面，允许均未造成蛋白质以成为膜结合，并阻断形成病毒颗粒。突变体G蛋白似乎不会在非智能温度下留下内质网，但这种缺陷是部分可逆的。在感染突变体的细胞中，使N蛋白迅速降解或将其组装成核胶囊，M蛋白没有与细胞表面成熟的膜和G蛋白结合，但从没有进入具有病毒密度的结构。导致M蛋白待降解的突变预防病毒粒子形成，G蛋白表现为N蛋白突变体感染的细胞中。这些结果与涉及已经在质膜中已经涉及可溶性核衣壳和可溶性M蛋白的可溶性核衣壳和可溶性M蛋白的组合模型。

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