COVID-19 感染的免疫表观遗传学见解。
An immune epigenetic insight to COVID-19 infection.
机构信息
Department of Biochemistry, All India Institute of Medical Sciences, New Delhi 110029, India.
Regional Institute of Ophthalmology, Institute of Medical Sciences, Banaras Hindu University, Varanasi 220115, India.
出版信息
Epigenomics. 2021 Mar;13(6):465-480. doi: 10.2217/epi-2020-0349. Epub 2021 Mar 9.
Severe acute respiratory syndrome coronavirus-2 is a positive-sense RNA virus, a causal agent of ongoing COVID-19 pandemic. methylation across three CpG sites (cg04013915, cg08559914, cg03536816) determines the host cell's entry. It regulates ACE2 expression by controlling the SIRT1 and KDM5B activity. Further, it regulates Type I and III IFN response by modulating H3K27me3 and H3K4me3 histone mark. SARS-CoV-2 protein with bromodomain and protein E mimics bromodomain histones and evades from host immune response. The 2'-O MTases mimics the host's cap1 structure and plays a vital role in immune evasion through Hsp90-mediated epigenetic process to hijack the infected cells. Although the current review highlighted the critical epigenetic events associated with SARS-CoV-2 immune evasion, the detailed mechanism is yet to be elucidated.
严重急性呼吸综合征冠状病毒 2 是一种正链 RNA 病毒，是持续 COVID-19 大流行的病原体。三个 CpG 位点（cg04013915、cg08559914、cg03536816）的甲基化决定了宿主细胞的进入。它通过控制 SIRT1 和 KDM5B 的活性来调节 ACE2 的表达。此外，它通过调节 H3K27me3 和 H3K4me3 组蛋白标记来调节 I 型和 III 型 IFN 反应。带有溴结构域和蛋白 E 的 SARS-CoV-2 蛋白模拟溴结构域组蛋白，并通过 HSP90 介导的表观遗传过程逃避宿主免疫反应。2'-O MTases 模拟宿主的 cap1 结构，并通过劫持感染细胞来发挥至关重要的免疫逃避作用。尽管目前的综述强调了与 SARS-CoV-2 免疫逃避相关的关键表观遗传事件，但详细的机制仍有待阐明。
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