Viruses have evolved strategies to ensure efficient translation using host cell ribosomes and translation factors. In addition to cleaving translation initiation factors required for host cell translation, poliovirus (PV) uses an internal ribosome entry site (IRES). Recent studies suggest that viruses exploit specific ribosomal proteins to enhance translation of their viral proteins. The ribosomal protein receptor for activated C kinase 1 (RACK1), a protein of the 40S ribosomal subunit, was previously shown to mediate translation from the 5' cricket paralysis virus and hepatitis C virus IRESs. Here we found that translation of a PV dual-luciferase reporter shows a moderate dependence on RACK1. However, in the context of a viral infection we observed significantly reduced poliovirus plaque size and titers and delayed host cell translational shut-off. Our findings further illustrate the involvement of the cellular translational machinery during PV infection and how viruses usurp the function of specific ribosomal proteins.

中文翻译：

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核糖体蛋白RACK1增强脊髓灰质炎病毒和其他病毒IRES的翻译。

病毒已经进化出策略，以确保使用宿主细胞核糖体和翻译因子进行有效翻译。除裂解宿主细胞翻译所需的翻译起始因子外，脊髓灰质炎病毒（PV）还使用内部核糖体进入位点（IRES）。最近的研究表明，病毒利用特定的核糖体蛋白来增强其病毒蛋白的翻译。先前显示，激活的C激酶1（RACK1）是40S核糖体亚基的蛋白质，其核糖体蛋白质受体介导5'cket瘫痪病毒和丙型肝炎病毒IRESs的翻译。在这里，我们发现PV双荧光素酶报告基因的翻译显示对RACK1的中等依赖性。然而，在病毒感染的情况下，我们观察到脊髓灰质炎病毒斑块大小和效价显着降低，并且宿主细胞翻译关闭延迟。我们的发现进一步说明了PV感染过程中细胞翻译机制的参与以及病毒如何篡夺特定核糖体蛋白的功能。