Table 1. Epigenetically upregulated receptors/mediators associated with SARS-CoV-2 entry.

Receptor/mediator	Role in COVID-19	Histone marks in mdig+ epithelial cells	Ref.
ACE2	The main receptor mediating SARS-CoV-2 entry, the expression of ACE2 is maintained, if not upregulated, as a result of the arsenic-induced impaired activity of EZH2.	↓ H3K27me3	[10,18,19]
NRP1	Highly expressed in the respiratory tract epithelial cells, NRP1 bind the S1 segment of the SARS-CoV-2 spike protein following its cleavage by furin.	↑ H3K4me3 ↓ H3K9me3	[10,20]
NRP2	Similar to NRP1.	↑ H3K4me3 ↓ H3K9me3 ↓ H3K27me3	[10,21]
AT1R	Facilitates SARS-CoV-2 entry through receptor-mediated endocytosis of sACE2-S complex following the interaction of viral spike protein with soluble ACE2.	↓ H3K9me3	[10,22,23]
CTSD	Potentially facilitates SARS-CoV-2 entry through positive regulation of furin by means of osteopontin.	↓ H3K9me3 ↓ H3K27me3	[10,24–26]
CTSL	Elevated in the serum of COVID-19 patients, CTSL mediates viral entry by participating in the cleavage of the viral S protein.	↑ H3K4me3 ↓ H3K9me3 ↓ H3K27me3	[10,27]
PTGER2-4	Upregulation of PGE2 receptors might potentiate the positive regulatory effect of PGE2 on ACE2 and TMPRSS2, facilitating SARS-CoV-2 entry.	↑ H3K4me3	[10,28,29]
SLC6A20/SIT1	Positively regulated by ACE2, SLC6A20/SIT1 is suspected to reciprocally interact with ACE2 and enhance its activity.	↓ H3K27me3	[10,30,31]
IL-6	Present in high levels in the serum of COVID-19 patients, IL-6 is speculated to enhance viral entry by activating the AT1R signaling cascade.	↓ H3K27me3	[4,23,32,33]