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| COVID-19 research v1.14 | CCR5 |
Sarah Leigh changed review comment from: CCR5 was identified through an OMIM search for potential viral susceptibility genes. Initial triage by Illumina (Alison Coffey and team) was given a Tier 3 grouping (experimental evidence and association data consistent with viral susceptibility); to: CCR5 was identified through an OMIM search for potential viral susceptibility genes. Initial triage by Illumina (Alison Coffey and team) was given a Tier 3 grouping (experimental evidence and association data consistent with viral susceptibility). Illumina review: Cytokine receptor. From OMIM: Variation in the CCR5 gene is associated with susceptibility to West Nile Virus (PMID 16230476;21935451;19247438). Numerous studies additionally demonstrate variation in CCR5 is associated with resistance / susceptibility to HIV and HBV infection. PMID 24098976: Zapata et al. (2013) - main genetic factor related to HIV-1 resistance is the CCR5-Δ32 variant. The CCR5-Δ32 variant along with SNPs in the CCR5 promoter and the CCR2-V64I variant have been included in seven human haplogroups (HH) previously associated with resistance/susceptibility to HIV-1 infection and different rates of AIDS progression. This study determined the association of the CCR5 promoter SNPs, the CCR5-Δ32 mutation, CCR2-V64I SNP, and HH frequencies with resistance/susceptibility to HIV-1 infection in a cohort of HIV-1-serodiscordant couples from Colombia. The CCR5-Δ32 allele is not responsible for HIV-1 resistance in this HESN group; however, the CCR2-I allele could be protective, while the 29G allele might increase the likelihood of acquiring HIV-1 infection. HHG1 and the AGACCAC-CCR2-I-CCR5 wild-type haplotype might promote HIV-1 infection while HHF2 might be related to resistance. PMID 31686727: Moudi et al. (2019) - study evaluated the association between the CCR5-Δ32, CCR5-2459A/G, MCP-1-2518A/G, VDR-APa1A/C, VDR-Taq1T/C SNPs and HBV susceptibility, in samples of Iranian populations. Significant associations with susceptibility to chronic HBV infection was observed with CCR5-2459A/G, MCP1-2518A/G, VDR-APa1A/C, VDR-Taq1T/C polymorphisms. In addition, no association of the CCR5D32 SNP with the disease was found. PMID:31100442 - Koor et al. (2019) - 9 CCR5 haplotypes are defined by seven 5'UTR SNPs in HIV-1 disease. Study identified key SNPs in HIV-1 control in both controllers and progressors. |
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| COVID-19 research v0.348 | CCR2 |
Rebecca Foulger changed review comment from: Evidence Summary from Illumina curation team: CCR2 is a chemokine receptor highly expressed on monocytes which is critical for bone marrow egress of classic monocytes and trafficking to sites of inflammation. Ccr2 deficiency in mice markedly increases mortality in West Nile virus encephalitis, with Ccr2-/- mice showing sustained monocytopenia, reduced accumulation of monocytes in the brain and an increase in cerebral viral load (Lim et al, 2011). CCR2 has been reported to mediate increased susceptibility to post-H1N1 bacterial pneumonia by limiting dendritic cell induction of IL-17 (Gurczynski et al, 2019). Nine SNPs in the CCR2 gene have been associated with susceptibility to and severity of several diseases including HIV and hepatitis C virus infection (Stone et al, 2017 Review; Ngoufack et al, 2019). PMID: 21131425; Lim et al, 2011 - Ccr2-deficiency resulted in markedly increased mortality (~20% survival). This was associated with increased viral load in the CNS of Ccr2-deficient mice on day 12 post-infection. This appeared to be specific to the brain and not in the blood. Monocyte accumulation is strongly reduced in Ccr2-/- mice. Brain tissue from infected Ccr2−/− mice showed markedly fewer immunoreactive cells as evaluated by immunohistochemistry analysis (Fig4). PMID: 30498200; Gurczynski et al, 2019 - H1N1 infected CCR2−/− mice had significantly higher survival as compared to H1N1 infected WT mice which is associated with significantly improved bacterial clearance at 24 and 48 hours (10 fold and 14 fold, respectively) post-bacterial challenge (with MRSA). In comparison to WT H1N1 infected mice, CCR2−/− mice recruited ~3-fold more IL-17 producing γδ-T cells and ~2.5-fold more Th17 cells (Figure 4B). Expression of CCL2 (MCP-1) in the lung is increased following H1N1 infection or H1N1 / MRSA dual infection as measured via qRT-PCR (Fig1).; to: Evidence Summary from Illumina curation team: CCR2 is a chemokine receptor highly expressed on monocytes which is critical for bone marrow egress of classic monocytes and trafficking to sites of inflammation. Ccr2 deficiency in mice markedly increases mortality in West Nile virus encephalitis, with Ccr2-/- mice showing sustained monocytopenia, reduced accumulation of monocytes in the brain and an increase in cerebral viral load (Lim et al, 2011). CCR2 has been reported to mediate increased susceptibility to post-H1N1 bacterial pneumonia by limiting dendritic cell induction of IL-17 (Gurczynski et al, 2019). Nine SNPs in the CCR2 gene have been associated with susceptibility to and severity of several diseases including HIV and hepatitis C virus infection (Stone et al, 2017 Review; Ngoufack et al, 2019). PMID: 21131425; Lim et al, 2011 - Ccr2-deficiency resulted in markedly increased mortality (~20% survival). This was associated with increased viral load in the CNS of Ccr2-deficient mice on day 12 post-infection. This appeared to be specific to the brain and not in the blood. Monocyte accumulation is strongly reduced in Ccr2-/- mice. Brain tissue from infected Ccr2−/− mice showed markedly fewer immunoreactive cells as evaluated by immunohistochemistry analysis (Fig4). PMID: 30498200; Gurczynski et al, 2019 - H1N1 infected CCR2−/− mice had significantly higher survival as compared to H1N1 infected WT mice which is associated with significantly improved bacterial clearance at 24 and 48 hours (10 fold and 14 fold, respectively) post-bacterial challenge (with MRSA). In comparison to WT H1N1 infected mice, CCR2−/− mice recruited ~3-fold more IL-17 producing γδ-T cells and ~2.5-fold more Th17 cells (Figure 4B). Expression of CCL2 (MCP-1) in the lung is increased following H1N1 infection or H1N1 / MRSA dual infection as measured via qRT-PCR (Fig1). |
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| COVID-19 research v0.348 | CCR2 |
Rebecca Foulger changed review comment from: Evidence Summary from Illumina curation team: CCR2 is a chemokine receptor highly expressed on monocytes which is critical for bone marrow egress of classic monocytes and trafficking to sites of inflammation. Ccr2 deficiency in mice markedly increases mortality in West Nile virus encephalitis, with Ccr2-/- mice showing sustained monocytopenia, reduced accumulation of monocytes in the brain and an increase in cerebral viral load (Lim et al, 2011). CCR2 has been reported to mediate increased susceptibility to post-H1N1 bacterial pneumonia by limiting dendritic cell induction of IL-17 (Gurczynski et al, 2019). Nine SNPs in the CCR2 gene have been associated with susceptibility to and severity of several diseases including HIV and hepatitis C virus infection (Stone et al, 2017 Review; Ngoufack et al, 2019). PMID: 21131425; Lim et al, 2011 - Ccr2-deficiency resulted in markedly increased mortality (~20% survival). This was associated with increased viral load in the CNS of Ccr2-deficient mice on day 12 post-infection. This appeared to be specific to the brain and not in the blood. Monocyte accumulation is strongly reduced in Ccr2-/- mice. Brain tissue from infected Ccr2−/− mice showed markedly fewer immunoreactive cells as evaluated by immunohistochemistry analysis (Fig4). PMID: 30498200; Gurczynski et al, 2019 - H1N1 infected CCR2−/− mice had significantly higher survival as compared to H1N1 infected WT mice which is associated with significantly improved bacterial clearance at 24 and 48 hours (10 fold and 14 fold, respectively) post-bacterial challenge (with MRSA). In comparison to WT H1N1 infected mice, CCR2−/− mice recruited ~3-fold more IL-17 producing γδ-T cells and ~2.5-fold more Th17 cells (Figure 4B). Expression of CCL2 (MCP-1) in the lung is increased following H1N1 infection or H1N1 / MRSA dual infection as measured via qRT-PCR (Fig1).; to: Evidence Summary from Illumina curation team: CCR2 is a chemokine receptor highly expressed on monocytes which is critical for bone marrow egress of classic monocytes and trafficking to sites of inflammation. Ccr2 deficiency in mice markedly increases mortality in West Nile virus encephalitis, with Ccr2-/- mice showing sustained monocytopenia, reduced accumulation of monocytes in the brain and an increase in cerebral viral load (Lim et al, 2011). CCR2 has been reported to mediate increased susceptibility to post-H1N1 bacterial pneumonia by limiting dendritic cell induction of IL-17 (Gurczynski et al, 2019). Nine SNPs in the CCR2 gene have been associated with susceptibility to and severity of several diseases including HIV and hepatitis C virus infection (Stone et al, 2017 Review; Ngoufack et al, 2019). PMID: 21131425; Lim et al, 2011 - Ccr2-deficiency resulted in markedly increased mortality (~20% survival). This was associated with increased viral load in the CNS of Ccr2-deficient mice on day 12 post-infection. This appeared to be specific to the brain and not in the blood. Monocyte accumulation is strongly reduced in Ccr2-/- mice. Brain tissue from infected Ccr2−/− mice showed markedly fewer immunoreactive cells as evaluated by immunohistochemistry analysis (Fig4). PMID: 30498200; Gurczynski et al, 2019 - H1N1 infected CCR2−/− mice had significantly higher survival as compared to H1N1 infected WT mice which is associated with significantly improved bacterial clearance at 24 and 48 hours (10 fold and 14 fold, respectively) post-bacterial challenge (with MRSA). In comparison to WT H1N1 infected mice, CCR2−/− mice recruited ~3-fold more IL-17 producing γδ-T cells and ~2.5-fold more Th17 cells (Figure 4B). Expression of CCL2 (MCP-1) in the lung is increased following H1N1 infection or H1N1 / MRSA dual infection as measured via qRT-PCR (Fig1). |
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| COVID-19 research v0.348 | CCR2 | Rebecca Foulger changed review comment from: Identified through an OMIM search for potential viral susceptibility genes, and subsequently triaged/reviewed by Illumina curation team.; to: Identified through an OMIM search for potential viral susceptibility genes, and subsequently triaged/reviewed by Illumina curation team. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| COVID-19 research v0.348 | CCR2 |
Rebecca Foulger commented on gene: CCR2: Evidence Summary from Illumina curation team: CCR2 is a chemokine receptor highly expressed on monocytes which is critical for bone marrow egress of classic monocytes and trafficking to sites of inflammation. Ccr2 deficiency in mice markedly increases mortality in West Nile virus encephalitis, with Ccr2-/- mice showing sustained monocytopenia, reduced accumulation of monocytes in the brain and an increase in cerebral viral load (Lim et al, 2011). CCR2 has been reported to mediate increased susceptibility to post-H1N1 bacterial pneumonia by limiting dendritic cell induction of IL-17 (Gurczynski et al, 2019). Nine SNPs in the CCR2 gene have been associated with susceptibility to and severity of several diseases including HIV and hepatitis C virus infection (Stone et al, 2017 Review; Ngoufack et al, 2019). PMID: 21131425; Lim et al, 2011 - Ccr2-deficiency resulted in markedly increased mortality (~20% survival). This was associated with increased viral load in the CNS of Ccr2-deficient mice on day 12 post-infection. This appeared to be specific to the brain and not in the blood. Monocyte accumulation is strongly reduced in Ccr2-/- mice. Brain tissue from infected Ccr2−/− mice showed markedly fewer immunoreactive cells as evaluated by immunohistochemistry analysis (Fig4). PMID: 30498200; Gurczynski et al, 2019 - H1N1 infected CCR2−/− mice had significantly higher survival as compared to H1N1 infected WT mice which is associated with significantly improved bacterial clearance at 24 and 48 hours (10 fold and 14 fold, respectively) post-bacterial challenge (with MRSA). In comparison to WT H1N1 infected mice, CCR2−/− mice recruited ~3-fold more IL-17 producing γδ-T cells and ~2.5-fold more Th17 cells (Figure 4B). Expression of CCL2 (MCP-1) in the lung is increased following H1N1 infection or H1N1 / MRSA dual infection as measured via qRT-PCR (Fig1). |
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| COVID-19 research v0.341 | CCR2 | Alison Coffey reviewed gene: CCR2: Rating: GREEN; Mode of pathogenicity: ; Publications: 21131425, 30498200, 28178200, 31777682; Phenotypes: ; Mode of inheritance: | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| COVID-19 research v0.336 | CCR2 | Rebecca Foulger commented on gene: CCR2 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| COVID-19 research v0.333 | CCR2 |
Rebecca Foulger gene: CCR2 was added gene: CCR2 was added to COVID-19 research. Sources: Expert list,OMIM,Expert Review Green Mode of inheritance for gene: CCR2 was set to Unknown |
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| COVID-19 research v0.85 | CCL2 | Rebecca Foulger commented on gene: CCL2: PMID:29057937 (Chowdhury and Khan, 2017) report that SNPs of CCL2 (rs1024611G) and its receptor CCR2 (rs1799864A) significantly associated with Japanese encephalitis (JE) which may serve as possible genetic predisposing factor. JE is one of the major viral encephalitis in Asia and parts of Western Pacific. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| COVID-19 research v0.47 | CCL2 | Rebecca Foulger commented on gene: CCL2: PMID:27260136 (Kim et al., 2016) report that CCL2 ablation highly increased susceptibility to Japanese encephalitis, indicating that CCL2 plays an essential role in conferring protection against JE caused by JE virus (JEV) infection. They also note a surprising opposite effect for ablation of the CCR2 (the corresponding receptor). | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||