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.
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。
