Table 1 Overview of SARS-CoV-2 candidate receptors
Name | Physiological role | Evidence for its role as a SARS-CoV-2 receptor | Refs. | |
|---|---|---|---|---|
Preprint | Peer-reviewed | |||
ACE2 | Blood pressure regulation | Cryo-EM/crystal structures of ACE2 bound to the S RBD | ||
Enhanced infection after ACE2 overexpression in cells | ||||
Enhanced infection after human ACE2 expression in mice | ||||
Partial inhibition of infection after ACE2 KO in cells | ||||
HS | Signalling, cell adhesion | Direct interaction between HS and S (EM, SPR, pull-down, glycan array, column chromatography) | ||
Partial inhibition of infection after enzymatic HS removal or KO of HS synthesis enzymes in cells | ||||
NRP1 | Cardiovascular and nervous system development | Direct binding of NRP1 to the RRAR peptide in S (co-IP) | ||
Enhanced infection after NRP1 overexpression in cells | ||||
Partial inhibition of infection after NRP1 KO/KD or treatment with NRP1-specific antibody in cells | ||||
SRB1 | Lipid uptake receptor | Enhanced infection of cells after SCARB1 overexpression and reduced infection after SCARB1 KD in the presence of HDL. | ||
Axl | Growth factor signalling | Direct interaction of Axl with the S NTD (pull-down, BLI) Enhanced infection after AXL overexpression in ACE2-KO cells Partial inhibition of infection after AXL KO in cells | ||
Basigin | Spermatogenesis, vision, immune responses | Direct binding of basigin to S RBD (SPR, ELISA, co-IP, EM) Enhanced infection after human BSG expression in cells and mice Partial inhibition after human BSG KD in cells | ||
LDLRAD3, TMEM30A and CLEC4G | Unknown, flippase, glycan binding | Direct interaction with the S NTD (Co-IP) Enhanced infection after overexpression in cells Partial inhibition of infection after KD in cells | ||
CD209 and CLEC4M | Cell adhesion and pathogen recognition | Direct interaction with S (pull-down, dot blot, SPR, EM) | ||
Enhanced infection after overexpression in cells | ||||
ASGPR1 and Kremen protein 1 | Glycoprotein homeostasis/apoptosis | Direct interaction with S (co-IP) Enhanced infection after overexpression in cells | ||
Transferrin receptor (TfR) | Iron transport | Direct interaction of TfR with S and ACE2 (ELISA, SPR) Enhanced infection after human TF expression in mice | ||
HAVcr-1 (also known as KIM1 and TIM1) | Immune system regulation | Direct interaction between HAVcr-1 and S RBD (co-IP, FRET, MST) | ||
Inhibition of virosome uptake by anti-HAVcr-1 antibodies or HAVCR1 KO | ||||
BiP (also known as GRP78) | Protein folding | Direct interaction of GRP78 with S (co-IP) Partial inhibition of infection by anti-GRP78 antibodies | ||
Sialic acid | Signalling/adhesion | Direct interaction with S protein (BLI) | ||
