Genes,Reference (PMID/PMCID),Evidence
ACE2,32418199,Angiotensin-converting enzyme 2 (ACE2) has been established as the functional host receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
CCL2,15919935,SARS-CoV induced the expression of chemokines such as CXCL10/IFN-gamma-inducible protein 10 and CCL2/monocyte chemotactic protein 1 
CD40,24845462,"A poor virus-specific CD4 and CD8 T cell response is attributed to an inefficient immune activation by SARS-CoV-MA15, particularly of respiratory DC (rDCs), as shown by reduced expression of MHC-II, CD86 and CD40 on cells harvested from the lung"
CRP,32243911,In the early stage of COVID-19 CRP levels were positively correlated with lung lesions and could reflect disease severity.
CSF2,32513566,"In the short time since the emergence of COVID-19, numerous studies have described abnormal levels of the following cytokines and chemokines in the patients: IL-1, IL-2, IL-4, IL-6, IL-7, IL-10, IL-12, IL-13, IL-17, M-CSF, G-CSF, GM-CSF, IP-10, IFN-?, MCP-1, MIP 1-?, hepatocyte growth factor (HGF), TNF-?, and vascular endothelial growth factor (VEGF) "
CSF3,32513566,"In the short time since the emergence of COVID-19, numerous studies have described abnormal levels of the following cytokines and chemokines in the patients: IL-1, IL-2, IL-4, IL-6, IL-7, IL-10, IL-12, IL-13, IL-17, M-CSF, G-CSF, GM-CSF, IP-10, IFN-?, MCP-1, MIP 1-?, hepatocyte growth factor (HGF), TNF-?, and vascular endothelial growth factor (VEGF) "
CXCL10,28466096,"SARS-CoV-infected airway epithelial cells (AECs) also produce large amounts of CCL3, CCL5, CCL2, and CXCL10"
CXCL5,32446778," SARS-CoV-2 upregulated only five of them, (namely, CXCL10, IL6, CCL2, CXCL1, CXCL5"
DPP4,32224164,Antibodies directed against DPP4 inhibited human coronavirus-Erasmus Medical Center (hCoV-EMC) infection of primary human bronchial epithelial cells and Huh-7 cells.
FURIN,32362314,The host cell protease furin cleaves the SARS-CoV-2 spike protein at the S1/S2 site
IFNA10,26410416,The nucleocapsid protein (N protein) of SARS-CoV plays an important role in inhibition of type I interferon (IFN) production via an unknown mechanism
IFNA14,26410416,The nucleocapsid protein (N protein) of SARS-CoV plays an important role in inhibition of type I interferon (IFN) production via an unknown mechanism
IFNA16,26410416,The nucleocapsid protein (N protein) of SARS-CoV plays an important role in inhibition of type I interferon (IFN) production via an unknown mechanism
IFNA2,26410416,The nucleocapsid protein (N protein) of SARS-CoV plays an important role in inhibition of type I interferon (IFN) production via an unknown mechanism
IFNA21,26410416,The nucleocapsid protein (N protein) of SARS-CoV plays an important role in inhibition of type I interferon (IFN) production via an unknown mechanism
IFNA8,26410416,The nucleocapsid protein (N protein) of SARS-CoV plays an important role in inhibition of type I interferon (IFN) production via an unknown mechanism
IFNAR1,32275914, IFN-I are thus among the first cytokines produced during a viral infection. They are recognized by the IFNAR receptor present at the plasma membrane in most cell types.
IFNAR2,32275914, IFN-I are thus among the first cytokines produced during a viral infection. They are recognized by the IFNAR receptor present at the plasma membrane in most cell types.
IFNB1,15476870,Interferon-beta and Interferon-Gamma Synergistically Inhibit the Replication of Severe Acute Respiratory Syndrome-Associated Coronavirus (SARS-CoV)
IFNG,15476870,Interferon-beta and Interferon-Gamma Synergistically Inhibit the Replication of Severe Acute Respiratory Syndrome-Associated Coronavirus (SARS-CoV)
IKBKB,"25363990, 24656046","IKK2 primarily phosphorylates inhibitors of ?B (I?B?, I?B?, and I?B?), which are degraded by the proteasome after polyubiquitination. The degradation of the inhibitor allows nuclear translocation of NF-?B and regulation of target-gene transcription. Noncanonical NF-?B Pathway Controls the Production of Type I Interferons in Antiviral Innate Immunity"
IKBKE,"25363990, 24656046","After activation of the IKK complex, IKK2 primarily phosphorylates inhibitors of ?B (I?B?, I?B?, and I?B?), which are degraded by the proteasome after polyubiquitination.The degradation of the inhibitor allows nuclear translocation of NF-?B and regulation of target-gene transcription. Noncanonical NF-?B Pathway Controls the Production of Type I Interferons in Antiviral Innate Immunity"
IKBKG,"25363990, 24656046","The IKK complex encompasses the scaffold protein NF-?B essential modulator (NEMO, also known as IKK?) and two other IKKs, IKK1 (IKK?) and IKK2 (IKK?). After activation of the IKK complex, IKK2 primarily phosphorylates inhibitors of ?B (I?B?, I?B?, and I?B?), which are degraded by the proteasome after polyubiquitination."
IL10,32169119,"A few plasma cytokines and chemokines were observed ascended in COVID-19 patients, including IL-1, IL-2, IL-4, IL-7, IL-10, IL-12, IL-13, IL-17, GCSF, macrophage colony-stimulating factor (MCSF), IP-10, MCP-1, MIP-1?, hepatocyte growth factor (HGF), IFN-? and TNF-?"
IL1B,32291137,"Evidence suggests that CRS might play a major role in severe COVID-19. Inflammatory cytokines and chemokines, including interleukin-6 (IL-6), interleukin-1? (IL-1?), induced protein 10 (IP10) and monocyte chemoattractant protein-1 (MCP-1) were significantly elevated in COVID-19 patients, and some were more commonly seen in severe patients than in nonsevere patients"
IL6,32291137,Elevated IL-6 levels were observed in patients with SARS and were correlated with disease severity 
IL7,32169119,"A few plasma cytokines and chemokines were observed ascended in COVID-19 patients, including IL-1, IL-2, IL-4, IL-7, IL-10, IL-12, IL-13, IL-17, GCSF, macrophage colony-stimulating factor (MCSF), IP-10, MCP-1, MIP-1?, hepatocyte growth factor (HGF), IFN-? and TNF-?"
IL9,32561873,"Concentrations of IL-4, IL-9 and IL-13, which are associated with type 2 immunity, bronchial hypersensitivity and increased mucus production, are also high in patients with COVID-19"
IRF3,25093995,"The cellular pathways mediated by interferon regulatory factor (IRF)-3 and -7, activating transcription factor (ATF)-2/jun, activator protein (AP)-1, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-?B), and nuclear factor of activated T cells (NF-AT), are the main drivers of the inflammatory response triggered after viral infections, with NF-?B pathway the most frequently activated"
IRF7,25093995,"The cellular pathways mediated by interferon regulatory factor (IRF)-3 and -7, activating transcription factor (ATF)-2/jun, activator protein (AP)-1, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-?B), and nuclear factor of activated T cells (NF-AT), are the main drivers of the inflammatory response triggered after viral infections, with NF-?B pathway the most frequently activated"
IRF9,25093995,"Type I IFN signaling starts with its binding to IFNAR receptors at the cell surface, which leads to the activation of the JAK–STAT pathway . The members of the Janus Kinase (JAK) family JAK-1 and protein tyrosine kinase 2 (TYK-2) phosphorylate the signal transducer and activators of transcription (STATs) which become activated. Phosphorylated STAT1 and STAT2 recruit IRF-9, to form the IFN stimulated gene factor 3 (ISGF3) complex. The ISGF3 heterotrimer translocates to the nucleus and triggers the transcription of IFN-stimulated genes (ISGs) that will drive the antiviral response."
JAK1,25093995,"Type I IFN signaling starts with its binding to IFNAR receptors at the cell surface, which leads to the activation of the JAK–STAT pathway . The members of the Janus Kinase (JAK) family JAK-1 and protein tyrosine kinase 2 (TYK-2) phosphorylate the signal transducer and activators of transcription (STATs) which become activated. Phosphorylated STAT1 and STAT2 recruit IRF-9, to form the IFN stimulated gene factor 3 (ISGF3) complex. The ISGF3 heterotrimer translocates to the nucleus and triggers the transcription of IFN-stimulated genes (ISGs) that will drive the antiviral response."
MAP3K7,28933406,Phosphorylation of all three MAPK members has been detected in cells infected with SARS-CoV
MAPK1,22936401,"Results point to SARS ?C oV PL pro triggering TGF ??1 production via ubiquitin proteasome, p38 MAPK , and ERK 1/2?mediated signaling."
MAPK14,22936401,"Results point to SARS ?C oV PL pro triggering TGF ??1 production via ubiquitin proteasome, p38 MAPK , and ERK 1/2?mediated signaling."
MAPK3,28933406,Expression of SARS-CoV PLpro was shown to increase ERK1 ubiquitin-mediated degradation to suppress IFN-induced responses 
MYD88,19079579,MyD88 Is Required for Protection from Lethal Infection with a Mouse-Adapted SARS-CoV
NFKB1,24198408,Inhibition of NF-?B-mediated Inflammation in Severe Acute Respiratory Syndrome Coronavirus-Infected Mice Increases Survival
NFKB2,24198408,Inhibition of NF-?B-mediated Inflammation in Severe Acute Respiratory Syndrome Coronavirus-Infected Mice Increases Survival
NLRP3,32574259,"Due to this crucial role in triggering inflammatory response to infection, the NLRP3 inflammasome appears to be a potential drug target in the treatment of coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2"
PCSK1,32099652,"Diabetes is associated with an increase in furin, which is a type-1 membrane-bound protease, belonging to the proprotein convertase subtilisin/kexin family (PCSK). It is involved in the entry of coronaviruses into the cell and increased Furin has been reported in diabetes, which might facilitate viral replication"
PCSK2,32099652,"Diabetes is associated with an increase in furin, which is a type-1 membrane-bound protease, belonging to the proprotein convertase subtilisin/kexin family (PCSK). It is involved in the entry of coronaviruses into the cell and increased Furin has been reported in diabetes, which might facilitate viral replication"
PCSK5,PMC7122180," the furin-like PCs PACE4, PC5, and PC7 may selectively compensate the activation of viral glycoproteins in furin-deficient cells and tissues with different efficiencies."
PCSK7,PMC7122180," the furin-like PCs PACE4, PC5, and PC7 may selectively compensate the activation of viral glycoproteins in furin-deficient cells and tissues with different efficiencies."
PIAS1,PMC7129356,The nucleocapsid protein of SARS CoV interacts with PIAS1 and affects the NFkappaB pathway
PIAS3,9724754 ,Inhibition of Stat1-mediated Gene Activation by PIAS1
REL,28933406,"Mammalian NF-?B family composes of five members, RelA (also named p65), RelB, c-Rel, NF-?B1 p50, and NF-?B2 p52, which form dimers in the cytoplasm,A recent study reported an enhanced nuclear NF-?B activity in PBMCs treated with a purified and recombinant SARS-CoV S protein"
RELA,28933406,"Mammalian NF-?B family composes of five members, RelA (also named p65), RelB, c-Rel, NF-?B1 p50, and NF-?B2 p52, which form dimers in the cytoplasm,A recent study reported an enhanced nuclear NF-?B activity in PBMCs treated with a purified and recombinant SARS-CoV S protein"
RELB,28933406,"Mammalian NF-?B family composes of five members, RelA (also named p65), RelB, c-Rel, NF-?B1 p50, and NF-?B2 p52, which form dimers in the cytoplasm,A recent study reported an enhanced nuclear NF-?B activity in PBMCs treated with a purified and recombinant SARS-CoV S protein"
SOCS3,16482545,Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6
STAT1,25093995,"Type I IFN signaling starts with its binding to IFNAR receptors at the cell surface, which leads to the activation of the JAK–STAT pathway (Samuel, 2001) (Fig. 2 ). The members of the Janus Kinase (JAK) family JAK-1 and protein tyrosine kinase 2 (TYK-2) phosphorylate the signal transducer and activators of transcription (STATs) which become activated. Phosphorylated STAT1 and STAT2 recruit IRF-9, to form the IFN stimulated gene factor 3 (ISGF3) complex. The ISGF3 heterotrimer translocates to the nucleus and triggers the transcription of IFN-stimulated genes (ISGs) that will drive the antiviral response."
STAT2,25093995,"Type I IFN signaling starts with its binding to IFNAR receptors at the cell surface, which leads to the activation of the JAK–STAT pathway (Samuel, 2001) (Fig. 2 ). The members of the Janus Kinase (JAK) family JAK-1 and protein tyrosine kinase 2 (TYK-2) phosphorylate the signal transducer and activators of transcription (STATs) which become activated. Phosphorylated STAT1 and STAT2 recruit IRF-9, to form the IFN stimulated gene factor 3 (ISGF3) complex. The ISGF3 heterotrimer translocates to the nucleus and triggers the transcription of IFN-stimulated genes (ISGs) that will drive the antiviral response."
STAT3,26199948,Severe acute respiratory syndrome coronavirus (SARS-CoV) infection results in STAT3 dephosphorylation.
TBK1,25093995,"ARS-CoV membrane (M) protein impairs the formation of TRAF3/TANK/TBK1/IKK? complex, inhibiting IFN-? production"
TLR3,26015500,Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus Infection
TLR7,32342146,The prominent ligand for TLR7 and 8 is viral ssRNA
TLR8,32342146,The prominent ligand for TLR7 and 8 is viral ssRNA
TMPRSS11D,32221306,"Expression of TMPRSS 2, 4, 11?A, 11D, and 11E on 293/hACE2 cells enhanced SARS-CoV-2 S protein-mediated cell–cell fusion similarly to SASR-CoV S "
TMPRSS11E,32221306,"Expression of TMPRSS 2, 4, 11?A, 11D, and 11E on 293/hACE2 cells enhanced SARS-CoV-2 S protein-mediated cell–cell fusion similarly to SASR-CoV S "
TMPRSS2,32221306,"Expression of TMPRSS 2, 4, 11?A, 11D, and 11E on 293/hACE2 cells enhanced SARS-CoV-2 S protein-mediated cell–cell fusion similarly to SASR-CoV S "
TMPRSS4,32221306,"Expression of TMPRSS 2, 4, 11?A, 11D, and 11E on 293/hACE2 cells enhanced SARS-CoV-2 S protein-mediated cell–cell fusion similarly to SASR-CoV S "
TRAF3,19380580,Severe Acute Respiratory Syndrome Coronavirus M Protein Inhibits Type I Interferon Production by Impeding the Formation of TRAF3·TANK·TBK1/IKK? Complex*
TRAF6,27164085,SARS Coronavirus Papain-Like Protease Inhibits the TLR7 Signaling Pathway Through Removing Lys63-Linked Polyubiquitination of TRAF3 and TRAF6
TYK2,25093995,"Type I IFN signaling starts with its binding to IFNAR receptors at the cell surface, which leads to the activation of the JAK–STAT pathway (Samuel, 2001) (Fig. 2 ). The members of the Janus Kinase (JAK) family JAK-1 and protein tyrosine kinase 2 (TYK-2) phosphorylate the signal transducer and activators of transcription (STATs) which become activated. Phosphorylated STAT1 and STAT2 recruit IRF-9, to form the IFN stimulated gene factor 3 (ISGF3) complex. The ISGF3 heterotrimer translocates to the nucleus and triggers the transcription of IFN-stimulated genes (ISGs) that will drive the antiviral response."