疹简单病毒pUL16和pUL21蛋白质阻止囊体与核孔复合体对接
Ethan C M Thomas1, Renée L Finnen1, Jeffrey D Mewburn2
1Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
PLoS pathogens
|December 1, 2023
概括
简单疹病毒 (HSV) 蛋白质pUL16和pUL21防止新组装的病毒囊重新进入细胞核. 这一发现澄清了HSV如何在宿主细胞内管理其复制周期.
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:
- 简单疹病毒 (HSV) 进入细胞,通过核孔综合体 (NPC) 将其基因组释放到细胞核中.
- 组装的病毒囊细胞移动到细胞质成熟,但防止它们重新进入细胞核的机制是未知的.
研究的目的:
- 调查新生的细胞质HSV核体与NPCs相互作用的机制.
- 确定参与调节核体贩运和核进口的病毒因素.
主要方法:
- 使用了简单疹病毒 (HSV) pUL16和pUL21删除突变.
- 在NPCs的细胞质面上观察到核体局部化在感染后期.
- 评估了pUL16和pUL21表达对传入核体对接和核输送的影响.
主要成果:
- HSV pUL16和pUL21删除突变显示在NPC中积累了空体.
- 对pUL16和pUL21的表达抑制了NPC中传入的核体的对接.
- pUL16和pUL21都局部存在于核外中,这表明它们在调节核体-NPC相互作用方面发挥了作用.
结论:
- HSV蛋白质pUL16和pUL21在防止细胞质核体重新进入细胞核中发挥着至关重要的作用.
- 这些病毒蛋白在核外处处于战略位置,以干扰核体-NPC相互作用.
- 了解这种机制可以了解HSV复制周期的调节.
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