An immune epigenetic insight to COVID-19 infection.
Bimal Prasad JitSahar QaziRakesh AryaAnkit SrivastavaNimesh GuptaAshok SharmaPublished in: Epigenomics (2021)
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.
Keyphrases
- sars cov
- respiratory syndrome coronavirus
- dna methylation
- immune response
- gene expression
- genome wide
- coronavirus disease
- binding protein
- induced apoptosis
- angiotensin ii
- angiotensin converting enzyme
- dendritic cells
- protein protein
- amino acid
- heat shock protein
- cell therapy
- signaling pathway
- single cell
- cell cycle arrest
- toll like receptor
- ischemia reperfusion injury
- endoplasmic reticulum stress
- long non coding rna
- cell death
- nucleic acid