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| COVID-19 research v0.349 | CXCL8 |
Rebecca Foulger commented on gene: CXCL8: Evidence Summary from Illumina curation team (Alison Coffey and Julie Taylor): • CXCL8 is a proinflammatory chemokine that plays a role in inflammatory response and immune cell trafficking • Multiple studies show IL-8 levels were shown to be elevated in plasma of patients with COVID-19, SARS-CoV, or MERS-CoV compared to controls. These include a number of recent COVID-19 studies (Coperchini et al. 2020). • Higher levels were detected in more severe cases (Gong et al. 2020; Qin et al. 2020; Yan et al. 2020), although one study shows the levels are within the normal range (Qin et al. 2020) • Gong et al. (2020) suggest that IL-8 might be a therapeutic target COVID-19 Literature: PMID 32446778; Coperchini et al. (2020) • Review article describing the involvement of chemokine/chemokine-receptor system in COVID-19 • Discusses the concept of cytokine storm where the immune system is ‘attacking’ the body resulting in acute respiratory distress syndrome. • Multiple studies are mentioned that show high levels of CXCL8 in the plasma and broncho-alveolar fluid in patients with acute respiratory distress syndrome. Reference a paper that notes that pre-treatment with an anti-CXCL8 antibody prevented acute lung injury that generally develops. • In vivo studies showed elevated CXCL8 in patients with SARS-CoV. • In vitro studies where peripheral blood mononuclear cells from healthy donor inoculated with SARS-CoV showed enhancement in the expression of CXCL8 • Similarly, CXCL8 was upregulated in cells lysates when with MERS-CoV infection of polarized airway epithelial cells (higher expression than SARS-CoV). • Higher plasma levels of CXCL8 in patients with COVID-19 compared to healthy controls; however, transcription of CSCL8 was not upregulated MedRxiv; Gong et al. (2020) • Evaluated disease severity in a total of 100 patients with COVID-19 pneumonia • CXCL8 (IL-8 in this paper) was detected in these patients and IL-8 levels were shown to be associated with disease severity (P<0.001); significant differences were noted between critical and severe patients or critical and mild groups (Tables 2 and 3) • Suggest that IL-8 might be a therapeutic target COVID-19 PMID 32161940; Qin et al. (2020) • Retrospective study of 452 patients with COVID-19; severity of COVID-19 defined according to the Fifth Revised Trial Version of the Novel Coronavirus Pneumonia Diagnosis and Treatment Guidance • Clinical and laboratory data were collected • A majority of the severe cases (n=286) had elevated levels of IL-8 (18.4 pg/mL vs 13.7 pg/mL, respectively; p<0.001) compared to the nonsevere cases (n=166), although they were all in the normal (0-62.0 pg/mL) (Table 2) MedRxiv; Yan et al. (2020) • Identified 25 genes that showed highly conserved kinetics in COVID-19 patients • Figure 3F shows expression of CXCL8 and plasma levels of IL-8 from four individuals with COVID-19 compared to four healthy controls was higher in patients especially in the severe stage (p<0.001) PMID 15585888; Chang et al. (2004) • Introduction has a summary of previously published papers and notes that high serum levels of IL-8 were detected during acute phase and associated with lung lesions in patients with SARS in one study. Another study suggests use of corticosteroids in reducing pulmonary inflammation due to IL-8. • Chang et al. (2004) used transient transfection of the SARS-CoV S protein-encoding plasmid on the IL-8 promoter. Measure of IL-8 release in lung cells showed an upregulation of IL-8 release. In addition, a specific region of the S protein was identified as a potentially important region for inducing IL-8 release. There are additional case-control studies suggesting possible association of polymorphisms in CXCL8 and acute bronchiolitis susceptibility (Pinto et al. 2017; PMID 27890033), asthma (Charrad et al. 2017; PMID 28993876), or human papillomavirus infection (weaker evidence; Junior et al. 2016; PMID 27783717). |
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| COVID-19 research v0.203 | ICOSLG | Sarah Leigh edited their review of gene: ICOSLG: Changed rating: RED | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| COVID-19 research v0.203 | ICOSLG | Sarah Leigh reviewed gene: ICOSLG: Rating: AMBER; Mode of pathogenicity: None; Publications: 30498080, 31532372; Phenotypes: ; Mode of inheritance: None | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| COVID-19 research v0.40 | ICOSLG |
Ellen McDonagh Source Expert Review Green was added to ICOSLG. Added phenotypes Immunodeficiencies affecting cellular and humoral immunity; Recurrent bacterial and viral infections for gene: ICOSLG Rating Changed from Red List (low evidence) to Green List (high evidence) |
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| COVID-19 research v0.36 | ICOSLG |
Ellen McDonagh gene: ICOSLG was added gene: ICOSLG was added to Viral susceptibility. Sources: Expert Review Red,Victorian Clinical Genetics Services,IUIS Classification December 2019 Mode of inheritance for gene: ICOSLG was set to BIALLELIC, autosomal or pseudoautosomal Publications for gene: ICOSLG were set to 32086639; 32048120; 30498080 Phenotypes for gene: ICOSLG were set to Immunodeficiencies affecting cellular and humoral immunity; Recurrent bacterial and viral infections |
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| COVID-19 research v0.36 | ICOS |
Ellen McDonagh gene: ICOS was added gene: ICOS was added to Viral susceptibility. Sources: Expert Review Green,ESID Registry 20171117,North West GLH,Victorian Clinical Genetics Services,GRID V2.0,NHS GMS,GOSH PID v.8.0,London North GLH,A- or hypo-gammaglobulinaemia v1.25,IUIS Classification February 2018 Mode of inheritance for gene: ICOS was set to BIALLELIC, autosomal or pseudoautosomal Publications for gene: ICOS were set to 15507387; 12577056; 29867948; 29226302; 24795713; 26399252; 25678089; 19380800; 28861081; 10413651; 29226301 Phenotypes for gene: ICOS were set to combined immunodeficiency; Isolated IgG subclass deficiency; gammaglobulinaemia; Immunodeficiency, common variable, 1, 607594; Immunodeficiencies affecting cellular and humoral immunity; Common variable immunodeficiency disorders (CVID); hypogammaglobulinaemia; Immunodeficiency, common variable, 1; Recurrent infections, autoimmunity, gastroenteritis, granulomas |
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