期刊
EPIGENOMICS
卷 13, 期 6, 页码 465-480出版社
FUTURE MEDICINE LTD
DOI: 10.2217/epi-2020-0349
关键词
ACE2; COVID-19; DNA methylation; histone PTMs; host-virus interaction; immune evasion; immunoepigenetics; SARS-CoV-2
资金
- Science and Engineering Research Board, DST, India [IPA/2020/000077]
This study highlights the critical epigenetic events associated with immune evasion of SARS-CoV-2, including ACE2R methylation, regulation of interferon response, and mimicry of histones, but the detailed mechanisms remain to be elucidated.
Severe acute respiratory syndrome coronavirus-2 is a positive-sense RNA virus, a causal agent of ongoing COVID-19 pandemic. ACE2R 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.
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