流感核蛋白中的免疫疏散性proline 283替代增加了聚合倾向,但没有改变原生结构
bioRxiv : the preprint server for biology
|September 25, 2023
概括
流感核蛋白 (NP) 突变,如Pro283,导致折叠缺陷并增加聚合. 这使得病毒独特地依赖宿主陪伴者生存和免疫逃避.
科学领域:
- 病毒学 病毒学
- 结构生物学 结构生物学
- 宿主-病原体相互作用
背景情况:
- 流感核蛋白 (NP) 对于病毒RNA包装和贩运至关重要.
- 宿主限制因素,如MxA,针对NP抑制流感病毒复制.
- 流感已经进化了NP中的突变,如Pro283,以抵抗MxA,但这些可以损害病毒适应性.
结论:
- 替代Pro283引入了流感NP折叠的生物物理缺陷.
- 流感病毒已经演化为依赖宿主护卫,以促进其他不稳定的病毒蛋白质的折叠.
- 这种对宿主陪伴者的依赖可能是一种逃避天生的免疫反应的机制.
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