在β型冠状病毒核体蛋白中,G3BP1结合基因的融合进化
Cinzia Borgogna1, Ilaria Cislaghi1, Sarah Turati1
1Virology Unit, Department of Translational Medicine, University of Piemonte Orientale, Via Generale Solaroli 17, Novara (NO), 28100, Italy.
Virus evolution
|September 12, 2025
概括
贝塔冠状病毒通过破坏宿主压力颗粒来逃避免疫反应. 在SARS-CoV-2核体蛋白使用ITFG动机结合G3BP1,抑制压力颗粒组装病毒复制.
科学领域:
- 病毒学 病毒学
- 分子生物学分子生物学
- 进化生物学 进化生物学
背景情况:
- 贝塔冠状病毒 (β-CoV) 使用各种策略来抵消宿主抗病毒防御,但它们的进化起源和功能意义尚未完全理解.
- 压力颗粒 (SGs) 对于细胞抗病毒反应至关重要,并且是病毒针对免疫逃避的目标.
- 严重急性呼吸道综合征冠状病毒2 (SARS-CoV-2) 核体 (N) 蛋白与G3BP1相互作用,破坏SG,促进病毒复制.
研究的目的:
- 研究β-CoV N蛋白质中G3BP1结合基因的进化起源和功能相关性.
- 为了确定ITFG基因在不同β-CoV亚系中的分布.
- 探索病毒免疫逃避策略的融合进化.
主要方法:
- 来自各种β-CoVs的179N蛋白序列的序列分析.
- 遗传学分析以追踪特定动机的进化出现.
- 在体外和细胞内测试以评估病毒N蛋白质对G3BP1的结合.
主要成果:
- 对于G3BP1相互作用至关重要的ITFG基因在sarbecoviruses中被确定,但在MERS-CoV和embbecoviruses中没有.
- 在测试的CoV中,只有SARS-CoV-2 N蛋白在体外和感染细胞中显示出显著的G3BP1结合.
- 遗传学分析表明,sarbecoviruses和merbecovirus类中的ΦxFG基因独立出现,而merbecoviruses中的VGTF基因也结合G3BP1,这表明了趋同的进化.
结论:
- 结合G3BP1的ITFG/ΦxFG基因在不同的β-CoV血统中独立演变为一种免疫逃避策略.
- 病毒N蛋白与G3BP1的相互作用代表了破坏宿主抗病毒防御的融合机制.
- 这些基因的出现独立于其他病毒因素,如4a蛋白,它也抑制了SG的形成.
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