细胞-细胞融合限制了尼帕病毒葡萄糖蛋白诱导的未折叠蛋白质反应的激活
Paula Jordan1, Sören Heyer1, Julian Hüther1
1Institute of Virology, Philipps University Marburg, Marburg, Germany.
Journal of virology
|December 11, 2025
概括
尼帕病毒 (NiV) 糖蛋白激活了展开的蛋白质反应 (UPR) 途径. 然而,NiV诱导的细胞融合限制了UPR激活,防止了抗病毒效应并促进了病毒传播.
科学领域:
- 病毒学 病毒学
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 尼帕病毒 (NiV) 复制取决于宿主细胞机器的糖蛋白合成,可能诱导ER压力和未折叠蛋白质反应 (UPR).
- UPR可以具有亲病毒和抗病毒的作用,使其在NiV感染中的作用成为研究的关键领域.
- 之前的研究没有阐明NiV感染期间的UPR激活状态.
研究的目的:
- 调查NiV感染与宿主细胞展开的蛋白质反应 (UPR) 之间的相互作用.
- 确定 NiV 如何调节 UPR 激活,特别是预防抗病毒反应.
- 探索 NiV 糖蛋白在 UPR 激活和调节中的作用.
主要方法:
- 在NiV感染细胞中分析UPR目标基因表达.
- 对 NiV 糖蛋白 (F 和 G) 对 UPR 激活的表达效应的研究.
- 与NiV诱导的细胞融合 (syncytium形成) 相关的UPR激活的评估.
主要成果:
- NiV 糖蛋白 F 和 G 激活了 UPR 的 IRE1/XBP1 分支.
- 尼维感染不会导致后期阶段持续的UPR基因上调.
- 由于NiV糖蛋白的共同表达而增加的syncytium形成与减少的UPR激活相关,这种现象取决于融合.
结论:
- 尼维利用合成的形成作为依赖于融合的机制来限制UPR的激活,从而防止潜在的抗病毒作用.
- 这种新的机制表明,NiV诱导的细胞融合不仅促进了病毒的传播,还调节了ER压力.
- 了解这种相互作用,可以了解原病毒如何管理由它们自身的葡萄糖蛋白诱导的ER应激反应.
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