RNA螺旋酶DDX39A结合了 chikungunya 病毒 RNA 中的一种保存结构,以控制感染
Iulia Tapescu1, Frances Taschuk2, Swechha M Pokharel3
1Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA, USA; Biochemistry and Biophysics Graduate Group, University of Pennsylvania, Philadelphia, PA, USA.
Molecular cell
|November 10, 2023
概括
细胞蛋白DDX39A通过结合病毒RNA结构来抑制阿尔法病毒的复制. 这一发现揭示了控制阿尔法病毒感染的新机制.
科学领域:
- 病毒学 病毒学
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 阿尔法病毒是重新出现的关节动物传播的RNA病毒,其紧的基因组对于复制至关重要.
- 细胞RNA结合蛋白,如DExD-box (DDX) 螺旋酶,识别病毒RNA结构以控制感染.
- 全系列的抗病毒DDX及其已知的RNA结构尚未完全理解.
研究的目的:
- 为了识别针对alphavirus的新型抗病毒DExD-box (DDX) 螺旋酶.
- 阐明DDX39A抑制 chikungunya病毒 (CHIKV) 复制的机制.
- 描述DDX39A和CHIKV基因组RNA之间的相互作用.
主要方法:
- 基因查以识别抗病毒DDXs对奇孔古尼亚病毒 (CHIKV).
- 在CHIKV感染后对DDX39A的细胞局部化研究.
- 生物化学分析以确定DDX39A与CHIKV基因组RNA和特定RNA元素的结合.
主要成果:
- DDX39A被确定为抗CHIKV和其他α病毒的抗病毒因子.
- 在CHIKV感染期间,DDX39A从核转移到细胞质,抑制病毒复制,独立于干扰素路径.
- DDX39A直接与CHIKV基因组RNA的5'保存序列元素 (5'CSE) 结合,这对其抗病毒活性至关重要.
结论:
- DDX39A代表了以前未被识别的抗病毒宿主因子对抗阿尔法病毒.
- DDX39A与阿尔法病毒基因组RNA的5'CSE相互作用是控制感染的关键机制.
- 这项研究揭示了一种新型的细胞先天免疫层,可以抵抗阿尔法病毒的传播.
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