An immune epigenetic insight to COVID-19 infection

• Published in: Epigenomics Vol. 13; no. 6; pp. 465 - 480
• Main Authors: Jit, Bimal P, Qazi, Sahar, Arya, Rakesh, Srivastava, Ankit, Gupta, Nimesh, Sharma, Ashok
• Format: Journal Article
• Language: English
• Published: England Future Medicine Ltd 01.03.2021
• Subjects: ACE2; Angiotensin-Converting Enzyme 2 - genetics; Antigen Presentation; COVID-19; COVID-19 - genetics; COVID-19 - immunology; DNA Methylation; Epigenesis, Genetic; histone PTMs; Histones; host-virus interaction; HSP90 Heat-Shock Proteins - genetics; Humans; Immune Evasion; immunoepigenetics; Review; SARS-CoV-2; SARS-CoV-2 - physiology; Virus Internalization; COVID-19; immunoepigenetics; ACE2; SARS-CoV-2; immune evasion; DNA methylation; host-virus interaction; histone PTMs
• ISSN: 1750-1911; 1750-192X
• DOI: 10.2217/epi-2020-0349

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.