CCR4-NOT有差异性地控制宿主与病毒的多尾长,并调节HCMV感染
Hannah M Burgess1,2, Rebecca Grande2, Sofia Riccio1
1Department of Microbial Sciences, University of Surrey, Guildford, UK.
EMBO reports
|October 17, 2023
概括
人类细胞巨核病毒 (HCMV) 在没有mRNA衰变酶的情况下重塑宿主基因表达. 宿主因子CNOT1和CNOT3通过调节病毒mRNA多A尾对HCMV复制至关重要.
科学领域:
- 病毒学 病毒学
- 分子生物学分子生物学
- 基因表达规范 基因表达规范
背景情况:
- 大多数病毒诱导mRNA衰变,但人类细胞巨核病毒 (HCMV) 以不同的方式重塑转基因组.
- HCMV感染会改变宿主基因表达,而不会产生自己的mRNA衰变酶.
研究的目的:
- 为了确定调节HCMV繁殖的宿主因素.
- 阐明HCMV颠覆细胞mRNA代谢的机制.
主要方法:
- 在人类原发性纤维细胞中准功能丧失的查.
- 纳米孔直接RNA测序以描述病毒和宿主mRNA的多个A尾长.
主要成果:
- 鉴定出CCR4-NOT死亡酶复合物的CNOT1和CNOT3是亲病毒宿主因素.
- CNOT1对于病毒晚期基因表达和受损细胞中宿主反应至关重要.
- 病毒mRNA具有比宿主mRNA更长的多A尾,对CCR4-NOT破坏不太敏感.
结论:
- 宿主CCR4-NOT介导的mRNA死亡化对于有效的HCMV复制至关重要.
- 冠状病毒感染通过一种新的机制颠覆了细胞mRNA代谢.
- CNOT1和CNOT3是抗HCMV策略的潜在治疗点.
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