With their categorical requirement for host ribosomes to translate mRNA, viruses provide a wealth of genetically tractable models to investigate how gene expression is remodeled post-transcriptionally by infection-triggered biological stress. By co-opting and subverting cellular pathways that control mRNA decay, modification, and translation, the global landscape of post-transcriptional processes is swiftly reshaped by virus-encoded factors. Concurrent host cell-intrinsic countermeasures likewise conscript post-transcriptional strategies to mobilize critical innate immune defenses. Here we review strategies and mechanisms that control mRNA decay, modification, and translation in animal virus-infected cells. Besides settling infection outcomes, post-transcriptional gene regulation in virus-infected cells epitomizes fundamental physiological stress responses in health and disease.

中文翻译：

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注意信息：控制病毒感染细胞中 RNA 衰变、修饰和翻译的策略

由于它们对宿主核糖体翻译 mRNA 的明确要求，病毒提供了丰富的遗传易处理模型来研究基因表达是如何通过感染触发的生物应激在转录后重塑的。通过选择和颠覆控制 mRNA 衰变、修饰和翻译的细胞通路，转录后过程的全球格局迅速被病毒编码因子重塑。并发的宿主细胞内在对策同样要求转录后策略来调动关键的先天免疫防御。在这里，我们回顾了在动物病毒感染的细胞中控制 mRNA 衰变、修饰和翻译的策略和机制。除了解决感染结果，