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CD27 and COVID-19 are reported together in 3 articles.

Gene

CD27

HGNC
HGNC:11922
5articles
5mentions
0variants with confirmed gene link
Most co-reported phenotypes (articles)
Phenotype

COVID-19

1,317articles
1,317mentions
12co-reported genes shown
Most co-reported genes (articles)

Counts are literature co-mentions in SaudiVarKB, not clinical or causal assertions. Gene details: HGNC; variant status: ClinVar via dbSNP.

Publications

3 records shown · first 60

Increased Activation Markers of Adaptive Immunity in Patients with Severe COVID-19.

PMID 39407725 | PMCID PMC11477269 | DOI 10.3390/jcm13195664 · Journal of clinical medicine · 2024 · 5 validated mentions
TypeEntitySource evidenceConfidenceExtractor
geneCD27“The expression of activation markers on B (CD27 and CD38) and T cells (CD27 and HLA-DR) was obtained using the flow cytometry technique.”0.98hgnc_dict_v1
phenotypeCOVID-19“Increased Activation Markers of Adaptive Immunity in Patients with Severe COVID-19.”0.98phenotype_alias_lexicon_v2
geneCD38“The expression of activation markers on B (CD27 and CD38) and T cells (CD27 and HLA-DR) was obtained using the flow cytometry technique.”0.98hgnc_dict_v1
geneCD19“Furthermore, the results revealed that severe COVID-19 patients had an increased frequency of CD19+ B cells, with changes in B cell subsets.”0.98hgnc_dict_v1

Role of CD27 and SAMHD1 and their genetic susceptibility to COVID-19.

PMID 38020556 | PMCID PMC10666556 | DOI 10.1016/j.sjbs.2023.103821 · Saudi journal of biological sciences · 2023 · 3 validated mentions
TypeEntitySource evidenceConfidenceExtractor
geneCD27“Role of CD27 and SAMHD1 and their genetic susceptibility to COVID-19.”0.98hgnc_dict_v1
phenotypeCOVID-19“Role of CD27 and SAMHD1 and their genetic susceptibility to COVID-19.”0.98phenotype_alias_lexicon_v2
geneSAMHD1“Role of CD27 and SAMHD1 and their genetic susceptibility to COVID-19.”0.98hgnc_dict_v1
TypeEntitySource evidenceConfidenceExtractor
geneCD27“Here, we hypothesize a potential anti-tumor immune response of SARS-CoV-2 and based on a computational approach show that: (i) SARS-CoV-2 Spike-RBD may bind to the extracellular domains of CD15, CD27, CD45, and CD152 receptors of cHL or FL and may directly inhibit cell proliferation. (ii) Alternately, upon internalization after binding to these CD molecules, the SARS-CoV-2 membrane (M) protein and ORF3a may bind to gamma-tubulin complex component 3 (GCP3) at its tubulin gamma-1 chain (TUBG1) binding site. (iii) The M protein may also interact with TUBG1, blocking its binding to GCP3. (iv) Both the M and ORF3a proteins may render the GCP2-GCP3 lateral binding where the M protein possibly interacts with GCP2 at its GCP3 binding site and the ORF3a protein to GCP3 at its GCP2 interacting residues. (v) Interactions of the M and ORF3a proteins with these gamma-tubulin ring complex components potentially block the initial process of microtubule nucleation, leading to cell-cycle arrest and apoptosis. (vi) The Spike-RBD may also interact with and block PD-1 signaling similar to pembrolizumab and nivolumab- like monoclonal antibodies and may induce B-cell apoptosis and remission. (vii) Finally, the TRADD interacting "PVQLSY" motif of Epstein-Barr virus LMP-1, that is responsible for NF-kB mediated oncogenesis, potentially interacts with SARS-CoV-2 Mpro, NSP7, NSP10, and spike (S) proteins, and may inhibit the LMP-1 mediated cell proliferation.”0.98hgnc_dict_v1
phenotypeCOVID-19“Recently, two cases of complete remission of classical Hodgkin lymphoma (cHL) and follicular lymphoma (FL) after SARS-CoV-2 infection were reported.”0.93phenotype_alias_lexicon_v2
geneTUBG1“Here, we hypothesize a potential anti-tumor immune response of SARS-CoV-2 and based on a computational approach show that: (i) SARS-CoV-2 Spike-RBD may bind to the extracellular domains of CD15, CD27, CD45, and CD152 receptors of cHL or FL and may directly inhibit cell proliferation. (ii) Alternately, upon internalization after binding to these CD molecules, the SARS-CoV-2 membrane (M) protein and ORF3a may bind to gamma-tubulin complex component 3 (GCP3) at its tubulin gamma-1 chain (TUBG1) binding site. (iii) The M protein may also interact with TUBG1, blocking its binding to GCP3. (iv) Both the M and ORF3a proteins may render the GCP2-GCP3 lateral binding where the M protein possibly interacts with GCP2 at its GCP3 binding site and the ORF3a protein to GCP3 at its GCP2 interacting residues. (v) Interactions of the M and ORF3a proteins with these gamma-tubulin ring complex components potentially block the initial process of microtubule nucleation, leading to cell-cycle arrest and apoptosis. (vi) The Spike-RBD may also interact with and block PD-1 signaling similar to pembrolizumab and nivolumab- like monoclonal antibodies and may induce B-cell apoptosis and remission. (vii) Finally, the TRADD interacting "PVQLSY" motif of Epstein-Barr virus LMP-1, that is responsible for NF-kB mediated oncogenesis, potentially interacts with SARS-CoV-2 Mpro, NSP7, NSP10, and spike (S) proteins, and may inhibit the LMP-1 mediated cell proliferation.”0.98hgnc_dict_v1
geneTRADD“Here, we hypothesize a potential anti-tumor immune response of SARS-CoV-2 and based on a computational approach show that: (i) SARS-CoV-2 Spike-RBD may bind to the extracellular domains of CD15, CD27, CD45, and CD152 receptors of cHL or FL and may directly inhibit cell proliferation. (ii) Alternately, upon internalization after binding to these CD molecules, the SARS-CoV-2 membrane (M) protein and ORF3a may bind to gamma-tubulin complex component 3 (GCP3) at its tubulin gamma-1 chain (TUBG1) binding site. (iii) The M protein may also interact with TUBG1, blocking its binding to GCP3. (iv) Both the M and ORF3a proteins may render the GCP2-GCP3 lateral binding where the M protein possibly interacts with GCP2 at its GCP3 binding site and the ORF3a protein to GCP3 at its GCP2 interacting residues. (v) Interactions of the M and ORF3a proteins with these gamma-tubulin ring complex components potentially block the initial process of microtubule nucleation, leading to cell-cycle arrest and apoptosis. (vi) The Spike-RBD may also interact with and block PD-1 signaling similar to pembrolizumab and nivolumab- like monoclonal antibodies and may induce B-cell apoptosis and remission. (vii) Finally, the TRADD interacting "PVQLSY" motif of Epstein-Barr virus LMP-1, that is responsible for NF-kB mediated oncogenesis, potentially interacts with SARS-CoV-2 Mpro, NSP7, NSP10, and spike (S) proteins, and may inhibit the LMP-1 mediated cell proliferation.”0.98hgnc_dict_v1