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疹病毒模仿细胞的基因组激活,以促进病毒复制

Florian Full¹, Stephanie Walter², Eva Neugebauer³

¹University Medical Center, and Faculty of Medicine, Albert-Ludwig-University Freiburg.

Research square

|January 3, 2024

概括

疹病毒和乳头瘤病毒激活DUX4基因,通常在成年人中被静止,以促进病毒复制. 这模仿了早期胚胎基因激活,这对于病毒生存和克服细胞防御是必不可少的.

科学领域:

分子生物学分子生物学
病毒学病毒学
遗传学是一个遗传学.

背景情况:

DUX4是早期胚胎基因激活的关键转录因子.
成人肌肉细胞中的DUX4调节失调会导致面骨肌肉发育不良 (FSHD).
病毒感染通常利用宿主细胞机械进行复制.

研究的目的:

为了研究DUX4在病毒感染中的作用.
为了确定病毒是否可以诱导DUX4表达.
阐明DUX4促进病毒复制的机制.

主要方法:

通过CRISPR/Cas9基因编辑来消耗DUX4.
病毒基因表达和复制的分析.
染色体免疫沉以评估DUX4与病毒基因组的结合.
涉及阿尔法,β和玛疹病毒和乳头瘤病毒的研究.
研究HSV-1直接早期蛋白质的作用.

主要成果:

疹病毒和乳头瘤病毒积极诱导DUX4的表达.
HSV-1蛋白直接对DUX4及其向基因进行上调,包括后置基因.
DUX4与病毒DNA结合,并增强病毒转录.
DUX4对于疹病毒复制是必不可少的;它的枯竭取消了病毒的传播.
病毒利用DUX4模仿胚胎转录,防止表观遗传沉默.

结论:

病毒劫持DUX4转录因子,以重新激活一个类似生殖系的程序.
这种DUX4介导的程序通过抵消表观遗传沉默来促进病毒基因表达和复制.
DUX4是疹病毒和其他潜在的病毒感染的关键宿主因子.

关键词:

DUX4X4 的使用情况这是EBV的EBV.这是FSHD的FSHD.这就是HCMV.这是一个HPVHPVHPV.在HSV-1病毒中,在HSV-2病毒中,疹病毒病毒的病毒.在 KSHVV 找 KSHV 它们是内生逆元件.紫毒基因组激活活动

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