PMC:7200337 / 54617-57296 JSONTXT

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    2_test

    {"project":"2_test","denotations":[{"id":"32505227-12692541-46575358","span":{"begin":685,"end":689},"obj":"12692541"},{"id":"32505227-17570115-46575359","span":{"begin":1232,"end":1236},"obj":"17570115"},{"id":"32505227-21958371-46575360","span":{"begin":1251,"end":1255},"obj":"21958371"},{"id":"32505227-21745520-46575361","span":{"begin":1270,"end":1274},"obj":"21745520"},{"id":"T65249","span":{"begin":685,"end":689},"obj":"12692541"},{"id":"T5000","span":{"begin":1232,"end":1236},"obj":"17570115"},{"id":"T67612","span":{"begin":1251,"end":1255},"obj":"21958371"},{"id":"T29548","span":{"begin":1270,"end":1274},"obj":"21745520"}],"text":"Susceptibility and Risk Biomarkers\nThere are currently limited known risk factors for susceptibility to COVID-19, although this has been evaluated in several studies. Zhao et al. compared the ABO blood group distribution in a cohort of 2,173 COVID-19 patients to that of healthy controls from the corresponding regions (Zhao et al., 2020b). They found blood group A to be associated with a higher risk for acquiring COVID-19 when compared to non-A blood groups; blood group O had the lowest risk for the infection. Another study demonstrated an identical association (Zietz and Tatonetti, 2020), and similar results have been previously described for other viruses (Lindesmith et al., 2003), including SARS-CoV-1 (Cheng et al., 2005a).\nSeveral large collaborative efforts are currently underway to generate, share, and analyze genetic data to understand the links between human genetic variation and COVID-19 susceptibility and severity, the most prominent of which is the COVID-19 Host Genetics Initiative (covid19hg.org). These studies are supported by previous observations on SARS-CoV-1 that followed the 2003 outbreak, which have identified significant associations between genetic variants and immune phenotypes (Chan et al., 2007, Wang et al., 2011, Zhao et al., 2011). Although identifying such polymorphisms and their associated genes and pathways for SARS-CoV-2 will require large cohorts, several studies, which remain to be tested in clinical trials, have already highlighted genetic polymorphisms that may potentially impact susceptibility. These studies have focused on genetic variants that may impact the expression or function of genes important in viral entry, namely ACE2 (SARS-CoV-2 receptor) and TMPRSS2 (spike protein activator) (Asselta et al., 2020, Cao et al., 2020c, Renieri et al., 2020, Stawiski et al., 2020). Cao et al. identified variants that are potentially expression quantitative trait loci (eQTL) of ACE2 (i.e., they may potentially alter ACE2 gene expression) and analyzed their frequencies in different populations (Cao et al., 2020c). Stawiski et al. listed variants that may be critical in ACE2 binding and thereby its function and compared the frequencies of these variants within different populations (Stawiski et al., 2020).\nWhile there are several limitations to these studies, the major question is whether the utility of these biomarkers is replicable in large populations with COVID-19 clinical outcomes data and in targeted or large-scale genomic analyses that are currently underway. In addition, these studies will reveal the potential associations between genetic variants and susceptibility in a gene or loci agnostic fashion."}

    LitCovid-PD-FMA-UBERON

    {"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T534","span":{"begin":196,"end":201},"obj":"Body_part"},{"id":"T535","span":{"begin":352,"end":357},"obj":"Body_part"},{"id":"T536","span":{"begin":448,"end":453},"obj":"Body_part"},{"id":"T537","span":{"begin":462,"end":467},"obj":"Body_part"},{"id":"T538","span":{"begin":1732,"end":1739},"obj":"Body_part"},{"id":"T539","span":{"begin":1980,"end":1984},"obj":"Body_part"},{"id":"T540","span":{"begin":2649,"end":2653},"obj":"Body_part"}],"attributes":[{"id":"A534","pred":"fma_id","subj":"T534","obj":"http://purl.org/sig/ont/fma/fma9670"},{"id":"A535","pred":"fma_id","subj":"T535","obj":"http://purl.org/sig/ont/fma/fma9670"},{"id":"A536","pred":"fma_id","subj":"T536","obj":"http://purl.org/sig/ont/fma/fma9670"},{"id":"A537","pred":"fma_id","subj":"T537","obj":"http://purl.org/sig/ont/fma/fma9670"},{"id":"A538","pred":"fma_id","subj":"T538","obj":"http://purl.org/sig/ont/fma/fma67257"},{"id":"A539","pred":"fma_id","subj":"T539","obj":"http://purl.org/sig/ont/fma/fma74402"},{"id":"A540","pred":"fma_id","subj":"T540","obj":"http://purl.org/sig/ont/fma/fma74402"}],"text":"Susceptibility and Risk Biomarkers\nThere are currently limited known risk factors for susceptibility to COVID-19, although this has been evaluated in several studies. Zhao et al. compared the ABO blood group distribution in a cohort of 2,173 COVID-19 patients to that of healthy controls from the corresponding regions (Zhao et al., 2020b). They found blood group A to be associated with a higher risk for acquiring COVID-19 when compared to non-A blood groups; blood group O had the lowest risk for the infection. Another study demonstrated an identical association (Zietz and Tatonetti, 2020), and similar results have been previously described for other viruses (Lindesmith et al., 2003), including SARS-CoV-1 (Cheng et al., 2005a).\nSeveral large collaborative efforts are currently underway to generate, share, and analyze genetic data to understand the links between human genetic variation and COVID-19 susceptibility and severity, the most prominent of which is the COVID-19 Host Genetics Initiative (covid19hg.org). These studies are supported by previous observations on SARS-CoV-1 that followed the 2003 outbreak, which have identified significant associations between genetic variants and immune phenotypes (Chan et al., 2007, Wang et al., 2011, Zhao et al., 2011). Although identifying such polymorphisms and their associated genes and pathways for SARS-CoV-2 will require large cohorts, several studies, which remain to be tested in clinical trials, have already highlighted genetic polymorphisms that may potentially impact susceptibility. These studies have focused on genetic variants that may impact the expression or function of genes important in viral entry, namely ACE2 (SARS-CoV-2 receptor) and TMPRSS2 (spike protein activator) (Asselta et al., 2020, Cao et al., 2020c, Renieri et al., 2020, Stawiski et al., 2020). Cao et al. identified variants that are potentially expression quantitative trait loci (eQTL) of ACE2 (i.e., they may potentially alter ACE2 gene expression) and analyzed their frequencies in different populations (Cao et al., 2020c). Stawiski et al. listed variants that may be critical in ACE2 binding and thereby its function and compared the frequencies of these variants within different populations (Stawiski et al., 2020).\nWhile there are several limitations to these studies, the major question is whether the utility of these biomarkers is replicable in large populations with COVID-19 clinical outcomes data and in targeted or large-scale genomic analyses that are currently underway. In addition, these studies will reveal the potential associations between genetic variants and susceptibility in a gene or loci agnostic fashion."}

    LitCovid-PD-UBERON

    {"project":"LitCovid-PD-UBERON","denotations":[{"id":"T57","span":{"begin":196,"end":201},"obj":"Body_part"},{"id":"T58","span":{"begin":352,"end":357},"obj":"Body_part"},{"id":"T59","span":{"begin":448,"end":453},"obj":"Body_part"},{"id":"T60","span":{"begin":462,"end":467},"obj":"Body_part"},{"id":"T61","span":{"begin":2482,"end":2487},"obj":"Body_part"}],"attributes":[{"id":"A57","pred":"uberon_id","subj":"T57","obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"A58","pred":"uberon_id","subj":"T58","obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"A59","pred":"uberon_id","subj":"T59","obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"A60","pred":"uberon_id","subj":"T60","obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"A61","pred":"uberon_id","subj":"T61","obj":"http://purl.obolibrary.org/obo/UBERON_0002542"}],"text":"Susceptibility and Risk Biomarkers\nThere are currently limited known risk factors for susceptibility to COVID-19, although this has been evaluated in several studies. Zhao et al. compared the ABO blood group distribution in a cohort of 2,173 COVID-19 patients to that of healthy controls from the corresponding regions (Zhao et al., 2020b). They found blood group A to be associated with a higher risk for acquiring COVID-19 when compared to non-A blood groups; blood group O had the lowest risk for the infection. Another study demonstrated an identical association (Zietz and Tatonetti, 2020), and similar results have been previously described for other viruses (Lindesmith et al., 2003), including SARS-CoV-1 (Cheng et al., 2005a).\nSeveral large collaborative efforts are currently underway to generate, share, and analyze genetic data to understand the links between human genetic variation and COVID-19 susceptibility and severity, the most prominent of which is the COVID-19 Host Genetics Initiative (covid19hg.org). These studies are supported by previous observations on SARS-CoV-1 that followed the 2003 outbreak, which have identified significant associations between genetic variants and immune phenotypes (Chan et al., 2007, Wang et al., 2011, Zhao et al., 2011). Although identifying such polymorphisms and their associated genes and pathways for SARS-CoV-2 will require large cohorts, several studies, which remain to be tested in clinical trials, have already highlighted genetic polymorphisms that may potentially impact susceptibility. These studies have focused on genetic variants that may impact the expression or function of genes important in viral entry, namely ACE2 (SARS-CoV-2 receptor) and TMPRSS2 (spike protein activator) (Asselta et al., 2020, Cao et al., 2020c, Renieri et al., 2020, Stawiski et al., 2020). Cao et al. identified variants that are potentially expression quantitative trait loci (eQTL) of ACE2 (i.e., they may potentially alter ACE2 gene expression) and analyzed their frequencies in different populations (Cao et al., 2020c). Stawiski et al. listed variants that may be critical in ACE2 binding and thereby its function and compared the frequencies of these variants within different populations (Stawiski et al., 2020).\nWhile there are several limitations to these studies, the major question is whether the utility of these biomarkers is replicable in large populations with COVID-19 clinical outcomes data and in targeted or large-scale genomic analyses that are currently underway. In addition, these studies will reveal the potential associations between genetic variants and susceptibility in a gene or loci agnostic fashion."}

    LitCovid-PD-MONDO

    {"project":"LitCovid-PD-MONDO","denotations":[{"id":"T351","span":{"begin":104,"end":112},"obj":"Disease"},{"id":"T352","span":{"begin":242,"end":250},"obj":"Disease"},{"id":"T353","span":{"begin":416,"end":424},"obj":"Disease"},{"id":"T354","span":{"begin":504,"end":513},"obj":"Disease"},{"id":"T355","span":{"begin":702,"end":710},"obj":"Disease"},{"id":"T356","span":{"begin":900,"end":908},"obj":"Disease"},{"id":"T357","span":{"begin":973,"end":981},"obj":"Disease"},{"id":"T358","span":{"begin":1080,"end":1088},"obj":"Disease"},{"id":"T359","span":{"begin":1361,"end":1369},"obj":"Disease"},{"id":"T360","span":{"begin":1692,"end":1700},"obj":"Disease"},{"id":"T361","span":{"begin":2425,"end":2433},"obj":"Disease"}],"attributes":[{"id":"A351","pred":"mondo_id","subj":"T351","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A352","pred":"mondo_id","subj":"T352","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A353","pred":"mondo_id","subj":"T353","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A354","pred":"mondo_id","subj":"T354","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A355","pred":"mondo_id","subj":"T355","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A356","pred":"mondo_id","subj":"T356","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A357","pred":"mondo_id","subj":"T357","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A358","pred":"mondo_id","subj":"T358","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A359","pred":"mondo_id","subj":"T359","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A360","pred":"mondo_id","subj":"T360","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A361","pred":"mondo_id","subj":"T361","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"}],"text":"Susceptibility and Risk Biomarkers\nThere are currently limited known risk factors for susceptibility to COVID-19, although this has been evaluated in several studies. Zhao et al. compared the ABO blood group distribution in a cohort of 2,173 COVID-19 patients to that of healthy controls from the corresponding regions (Zhao et al., 2020b). They found blood group A to be associated with a higher risk for acquiring COVID-19 when compared to non-A blood groups; blood group O had the lowest risk for the infection. Another study demonstrated an identical association (Zietz and Tatonetti, 2020), and similar results have been previously described for other viruses (Lindesmith et al., 2003), including SARS-CoV-1 (Cheng et al., 2005a).\nSeveral large collaborative efforts are currently underway to generate, share, and analyze genetic data to understand the links between human genetic variation and COVID-19 susceptibility and severity, the most prominent of which is the COVID-19 Host Genetics Initiative (covid19hg.org). These studies are supported by previous observations on SARS-CoV-1 that followed the 2003 outbreak, which have identified significant associations between genetic variants and immune phenotypes (Chan et al., 2007, Wang et al., 2011, Zhao et al., 2011). Although identifying such polymorphisms and their associated genes and pathways for SARS-CoV-2 will require large cohorts, several studies, which remain to be tested in clinical trials, have already highlighted genetic polymorphisms that may potentially impact susceptibility. These studies have focused on genetic variants that may impact the expression or function of genes important in viral entry, namely ACE2 (SARS-CoV-2 receptor) and TMPRSS2 (spike protein activator) (Asselta et al., 2020, Cao et al., 2020c, Renieri et al., 2020, Stawiski et al., 2020). Cao et al. identified variants that are potentially expression quantitative trait loci (eQTL) of ACE2 (i.e., they may potentially alter ACE2 gene expression) and analyzed their frequencies in different populations (Cao et al., 2020c). Stawiski et al. listed variants that may be critical in ACE2 binding and thereby its function and compared the frequencies of these variants within different populations (Stawiski et al., 2020).\nWhile there are several limitations to these studies, the major question is whether the utility of these biomarkers is replicable in large populations with COVID-19 clinical outcomes data and in targeted or large-scale genomic analyses that are currently underway. In addition, these studies will reveal the potential associations between genetic variants and susceptibility in a gene or loci agnostic fashion."}

    LitCovid-PD-CLO

    {"project":"LitCovid-PD-CLO","denotations":[{"id":"T665","span":{"begin":128,"end":131},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T666","span":{"begin":196,"end":201},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T667","span":{"begin":196,"end":201},"obj":"http://www.ebi.ac.uk/efo/EFO_0000296"},{"id":"T668","span":{"begin":224,"end":225},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T669","span":{"begin":352,"end":357},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T670","span":{"begin":352,"end":357},"obj":"http://www.ebi.ac.uk/efo/EFO_0000296"},{"id":"T671","span":{"begin":364,"end":365},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T672","span":{"begin":388,"end":389},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T673","span":{"begin":446,"end":447},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T674","span":{"begin":448,"end":453},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T675","span":{"begin":448,"end":453},"obj":"http://www.ebi.ac.uk/efo/EFO_0000296"},{"id":"T676","span":{"begin":462,"end":467},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T677","span":{"begin":462,"end":467},"obj":"http://www.ebi.ac.uk/efo/EFO_0000296"},{"id":"T678","span":{"begin":657,"end":664},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T679","span":{"begin":872,"end":877},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T680","span":{"begin":1338,"end":1343},"obj":"http://purl.obolibrary.org/obo/OGG_0000000002"},{"id":"T681","span":{"begin":1436,"end":1442},"obj":"http://purl.obolibrary.org/obo/UBERON_0000473"},{"id":"T682","span":{"begin":1573,"end":1580},"obj":"http://purl.obolibrary.org/obo/CLO_0009985"},{"id":"T683","span":{"begin":1647,"end":1652},"obj":"http://purl.obolibrary.org/obo/OGG_0000000002"},{"id":"T684","span":{"begin":1740,"end":1749},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T685","span":{"begin":1980,"end":1984},"obj":"http://purl.obolibrary.org/obo/OGG_0000000002"},{"id":"T686","span":{"begin":2647,"end":2648},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T687","span":{"begin":2649,"end":2653},"obj":"http://purl.obolibrary.org/obo/OGG_0000000002"}],"text":"Susceptibility and Risk Biomarkers\nThere are currently limited known risk factors for susceptibility to COVID-19, although this has been evaluated in several studies. Zhao et al. compared the ABO blood group distribution in a cohort of 2,173 COVID-19 patients to that of healthy controls from the corresponding regions (Zhao et al., 2020b). They found blood group A to be associated with a higher risk for acquiring COVID-19 when compared to non-A blood groups; blood group O had the lowest risk for the infection. Another study demonstrated an identical association (Zietz and Tatonetti, 2020), and similar results have been previously described for other viruses (Lindesmith et al., 2003), including SARS-CoV-1 (Cheng et al., 2005a).\nSeveral large collaborative efforts are currently underway to generate, share, and analyze genetic data to understand the links between human genetic variation and COVID-19 susceptibility and severity, the most prominent of which is the COVID-19 Host Genetics Initiative (covid19hg.org). These studies are supported by previous observations on SARS-CoV-1 that followed the 2003 outbreak, which have identified significant associations between genetic variants and immune phenotypes (Chan et al., 2007, Wang et al., 2011, Zhao et al., 2011). Although identifying such polymorphisms and their associated genes and pathways for SARS-CoV-2 will require large cohorts, several studies, which remain to be tested in clinical trials, have already highlighted genetic polymorphisms that may potentially impact susceptibility. These studies have focused on genetic variants that may impact the expression or function of genes important in viral entry, namely ACE2 (SARS-CoV-2 receptor) and TMPRSS2 (spike protein activator) (Asselta et al., 2020, Cao et al., 2020c, Renieri et al., 2020, Stawiski et al., 2020). Cao et al. identified variants that are potentially expression quantitative trait loci (eQTL) of ACE2 (i.e., they may potentially alter ACE2 gene expression) and analyzed their frequencies in different populations (Cao et al., 2020c). Stawiski et al. listed variants that may be critical in ACE2 binding and thereby its function and compared the frequencies of these variants within different populations (Stawiski et al., 2020).\nWhile there are several limitations to these studies, the major question is whether the utility of these biomarkers is replicable in large populations with COVID-19 clinical outcomes data and in targeted or large-scale genomic analyses that are currently underway. In addition, these studies will reveal the potential associations between genetic variants and susceptibility in a gene or loci agnostic fashion."}

    LitCovid-PD-CHEBI

    {"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T85513","span":{"begin":202,"end":207},"obj":"Chemical"},{"id":"T35249","span":{"begin":358,"end":363},"obj":"Chemical"},{"id":"T1068","span":{"begin":468,"end":473},"obj":"Chemical"},{"id":"T22429","span":{"begin":1732,"end":1739},"obj":"Chemical"}],"attributes":[{"id":"A80565","pred":"chebi_id","subj":"T85513","obj":"http://purl.obolibrary.org/obo/CHEBI_24433"},{"id":"A58886","pred":"chebi_id","subj":"T35249","obj":"http://purl.obolibrary.org/obo/CHEBI_24433"},{"id":"A62227","pred":"chebi_id","subj":"T1068","obj":"http://purl.obolibrary.org/obo/CHEBI_24433"},{"id":"A59004","pred":"chebi_id","subj":"T22429","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"}],"text":"Susceptibility and Risk Biomarkers\nThere are currently limited known risk factors for susceptibility to COVID-19, although this has been evaluated in several studies. Zhao et al. compared the ABO blood group distribution in a cohort of 2,173 COVID-19 patients to that of healthy controls from the corresponding regions (Zhao et al., 2020b). They found blood group A to be associated with a higher risk for acquiring COVID-19 when compared to non-A blood groups; blood group O had the lowest risk for the infection. Another study demonstrated an identical association (Zietz and Tatonetti, 2020), and similar results have been previously described for other viruses (Lindesmith et al., 2003), including SARS-CoV-1 (Cheng et al., 2005a).\nSeveral large collaborative efforts are currently underway to generate, share, and analyze genetic data to understand the links between human genetic variation and COVID-19 susceptibility and severity, the most prominent of which is the COVID-19 Host Genetics Initiative (covid19hg.org). These studies are supported by previous observations on SARS-CoV-1 that followed the 2003 outbreak, which have identified significant associations between genetic variants and immune phenotypes (Chan et al., 2007, Wang et al., 2011, Zhao et al., 2011). Although identifying such polymorphisms and their associated genes and pathways for SARS-CoV-2 will require large cohorts, several studies, which remain to be tested in clinical trials, have already highlighted genetic polymorphisms that may potentially impact susceptibility. These studies have focused on genetic variants that may impact the expression or function of genes important in viral entry, namely ACE2 (SARS-CoV-2 receptor) and TMPRSS2 (spike protein activator) (Asselta et al., 2020, Cao et al., 2020c, Renieri et al., 2020, Stawiski et al., 2020). Cao et al. identified variants that are potentially expression quantitative trait loci (eQTL) of ACE2 (i.e., they may potentially alter ACE2 gene expression) and analyzed their frequencies in different populations (Cao et al., 2020c). Stawiski et al. listed variants that may be critical in ACE2 binding and thereby its function and compared the frequencies of these variants within different populations (Stawiski et al., 2020).\nWhile there are several limitations to these studies, the major question is whether the utility of these biomarkers is replicable in large populations with COVID-19 clinical outcomes data and in targeted or large-scale genomic analyses that are currently underway. In addition, these studies will reveal the potential associations between genetic variants and susceptibility in a gene or loci agnostic fashion."}

    LitCovid-PD-GO-BP

    {"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T163","span":{"begin":1980,"end":1995},"obj":"http://purl.obolibrary.org/obo/GO_0010467"}],"text":"Susceptibility and Risk Biomarkers\nThere are currently limited known risk factors for susceptibility to COVID-19, although this has been evaluated in several studies. Zhao et al. compared the ABO blood group distribution in a cohort of 2,173 COVID-19 patients to that of healthy controls from the corresponding regions (Zhao et al., 2020b). They found blood group A to be associated with a higher risk for acquiring COVID-19 when compared to non-A blood groups; blood group O had the lowest risk for the infection. Another study demonstrated an identical association (Zietz and Tatonetti, 2020), and similar results have been previously described for other viruses (Lindesmith et al., 2003), including SARS-CoV-1 (Cheng et al., 2005a).\nSeveral large collaborative efforts are currently underway to generate, share, and analyze genetic data to understand the links between human genetic variation and COVID-19 susceptibility and severity, the most prominent of which is the COVID-19 Host Genetics Initiative (covid19hg.org). These studies are supported by previous observations on SARS-CoV-1 that followed the 2003 outbreak, which have identified significant associations between genetic variants and immune phenotypes (Chan et al., 2007, Wang et al., 2011, Zhao et al., 2011). Although identifying such polymorphisms and their associated genes and pathways for SARS-CoV-2 will require large cohorts, several studies, which remain to be tested in clinical trials, have already highlighted genetic polymorphisms that may potentially impact susceptibility. These studies have focused on genetic variants that may impact the expression or function of genes important in viral entry, namely ACE2 (SARS-CoV-2 receptor) and TMPRSS2 (spike protein activator) (Asselta et al., 2020, Cao et al., 2020c, Renieri et al., 2020, Stawiski et al., 2020). Cao et al. identified variants that are potentially expression quantitative trait loci (eQTL) of ACE2 (i.e., they may potentially alter ACE2 gene expression) and analyzed their frequencies in different populations (Cao et al., 2020c). Stawiski et al. listed variants that may be critical in ACE2 binding and thereby its function and compared the frequencies of these variants within different populations (Stawiski et al., 2020).\nWhile there are several limitations to these studies, the major question is whether the utility of these biomarkers is replicable in large populations with COVID-19 clinical outcomes data and in targeted or large-scale genomic analyses that are currently underway. In addition, these studies will reveal the potential associations between genetic variants and susceptibility in a gene or loci agnostic fashion."}

    LitCovid-PubTator

    {"project":"LitCovid-PubTator","denotations":[{"id":"1764","span":{"begin":192,"end":207},"obj":"Gene"},{"id":"1765","span":{"begin":439,"end":441},"obj":"Gene"},{"id":"1766","span":{"begin":366,"end":368},"obj":"Gene"},{"id":"1767","span":{"begin":260,"end":262},"obj":"Gene"},{"id":"1768","span":{"begin":101,"end":103},"obj":"Gene"},{"id":"1769","span":{"begin":251,"end":259},"obj":"Species"},{"id":"1770","span":{"begin":442,"end":447},"obj":"Species"},{"id":"1771","span":{"begin":702,"end":709},"obj":"Species"},{"id":"1772","span":{"begin":104,"end":112},"obj":"Disease"},{"id":"1773","span":{"begin":242,"end":250},"obj":"Disease"},{"id":"1774","span":{"begin":416,"end":424},"obj":"Disease"},{"id":"1775","span":{"begin":504,"end":513},"obj":"Disease"},{"id":"1791","span":{"begin":1686,"end":1690},"obj":"Gene"},{"id":"1792","span":{"begin":1717,"end":1724},"obj":"Gene"},{"id":"1793","span":{"begin":1726,"end":1731},"obj":"Gene"},{"id":"1794","span":{"begin":1936,"end":1940},"obj":"Gene"},{"id":"1795","span":{"begin":1975,"end":1979},"obj":"Gene"},{"id":"1796","span":{"begin":2130,"end":2134},"obj":"Gene"},{"id":"1797","span":{"begin":1430,"end":1432},"obj":"Gene"},{"id":"1798","span":{"begin":840,"end":842},"obj":"Gene"},{"id":"1799","span":{"begin":795,"end":797},"obj":"Gene"},{"id":"1800","span":{"begin":872,"end":877},"obj":"Species"},{"id":"1801","span":{"begin":1080,"end":1088},"obj":"Species"},{"id":"1802","span":{"begin":1361,"end":1371},"obj":"Species"},{"id":"1803","span":{"begin":1692,"end":1702},"obj":"Species"},{"id":"1804","span":{"begin":900,"end":908},"obj":"Disease"},{"id":"1805","span":{"begin":973,"end":981},"obj":"Disease"},{"id":"1808","span":{"begin":2305,"end":2307},"obj":"Gene"},{"id":"1809","span":{"begin":2425,"end":2433},"obj":"Disease"}],"attributes":[{"id":"A1764","pred":"tao:has_database_id","subj":"1764","obj":"Gene:28"},{"id":"A1765","pred":"tao:has_database_id","subj":"1765","obj":"Gene:6999"},{"id":"A1766","pred":"tao:has_database_id","subj":"1766","obj":"Gene:6999"},{"id":"A1767","pred":"tao:has_database_id","subj":"1767","obj":"Gene:6999"},{"id":"A1768","pred":"tao:has_database_id","subj":"1768","obj":"Gene:6999"},{"id":"A1769","pred":"tao:has_database_id","subj":"1769","obj":"Tax:9606"},{"id":"A1770","pred":"tao:has_database_id","subj":"1770","obj":"Tax:12440"},{"id":"A1771","pred":"tao:has_database_id","subj":"1771","obj":"Tax:694009"},{"id":"A1772","pred":"tao:has_database_id","subj":"1772","obj":"MESH:C000657245"},{"id":"A1773","pred":"tao:has_database_id","subj":"1773","obj":"MESH:C000657245"},{"id":"A1774","pred":"tao:has_database_id","subj":"1774","obj":"MESH:C000657245"},{"id":"A1775","pred":"tao:has_database_id","subj":"1775","obj":"MESH:D007239"},{"id":"A1791","pred":"tao:has_database_id","subj":"1791","obj":"Gene:59272"},{"id":"A1792","pred":"tao:has_database_id","subj":"1792","obj":"Gene:7113"},{"id":"A1793","pred":"tao:has_database_id","subj":"1793","obj":"Gene:43740568"},{"id":"A1794","pred":"tao:has_database_id","subj":"1794","obj":"Gene:59272"},{"id":"A1795","pred":"tao:has_database_id","subj":"1795","obj":"Gene:59272"},{"id":"A1796","pred":"tao:has_database_id","subj":"1796","obj":"Gene:59272"},{"id":"A1797","pred":"tao:has_database_id","subj":"1797","obj":"Gene:6999"},{"id":"A1798","pred":"tao:has_database_id","subj":"1798","obj":"Gene:6999"},{"id":"A1799","pred":"tao:has_database_id","subj":"1799","obj":"Gene:6999"},{"id":"A1800","pred":"tao:has_database_id","subj":"1800","obj":"Tax:9606"},{"id":"A1801","pred":"tao:has_database_id","subj":"1801","obj":"Tax:694009"},{"id":"A1802","pred":"tao:has_database_id","subj":"1802","obj":"Tax:2697049"},{"id":"A1803","pred":"tao:has_database_id","subj":"1803","obj":"Tax:2697049"},{"id":"A1804","pred":"tao:has_database_id","subj":"1804","obj":"MESH:C000657245"},{"id":"A1805","pred":"tao:has_database_id","subj":"1805","obj":"MESH:C000657245"},{"id":"A1808","pred":"tao:has_database_id","subj":"1808","obj":"Gene:6999"},{"id":"A1809","pred":"tao:has_database_id","subj":"1809","obj":"MESH:C000657245"}],"namespaces":[{"prefix":"Tax","uri":"https://www.ncbi.nlm.nih.gov/taxonomy/"},{"prefix":"MESH","uri":"https://id.nlm.nih.gov/mesh/"},{"prefix":"Gene","uri":"https://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"CVCL","uri":"https://web.expasy.org/cellosaurus/CVCL_"}],"text":"Susceptibility and Risk Biomarkers\nThere are currently limited known risk factors for susceptibility to COVID-19, although this has been evaluated in several studies. Zhao et al. compared the ABO blood group distribution in a cohort of 2,173 COVID-19 patients to that of healthy controls from the corresponding regions (Zhao et al., 2020b). They found blood group A to be associated with a higher risk for acquiring COVID-19 when compared to non-A blood groups; blood group O had the lowest risk for the infection. Another study demonstrated an identical association (Zietz and Tatonetti, 2020), and similar results have been previously described for other viruses (Lindesmith et al., 2003), including SARS-CoV-1 (Cheng et al., 2005a).\nSeveral large collaborative efforts are currently underway to generate, share, and analyze genetic data to understand the links between human genetic variation and COVID-19 susceptibility and severity, the most prominent of which is the COVID-19 Host Genetics Initiative (covid19hg.org). These studies are supported by previous observations on SARS-CoV-1 that followed the 2003 outbreak, which have identified significant associations between genetic variants and immune phenotypes (Chan et al., 2007, Wang et al., 2011, Zhao et al., 2011). Although identifying such polymorphisms and their associated genes and pathways for SARS-CoV-2 will require large cohorts, several studies, which remain to be tested in clinical trials, have already highlighted genetic polymorphisms that may potentially impact susceptibility. These studies have focused on genetic variants that may impact the expression or function of genes important in viral entry, namely ACE2 (SARS-CoV-2 receptor) and TMPRSS2 (spike protein activator) (Asselta et al., 2020, Cao et al., 2020c, Renieri et al., 2020, Stawiski et al., 2020). Cao et al. identified variants that are potentially expression quantitative trait loci (eQTL) of ACE2 (i.e., they may potentially alter ACE2 gene expression) and analyzed their frequencies in different populations (Cao et al., 2020c). Stawiski et al. listed variants that may be critical in ACE2 binding and thereby its function and compared the frequencies of these variants within different populations (Stawiski et al., 2020).\nWhile there are several limitations to these studies, the major question is whether the utility of these biomarkers is replicable in large populations with COVID-19 clinical outcomes data and in targeted or large-scale genomic analyses that are currently underway. In addition, these studies will reveal the potential associations between genetic variants and susceptibility in a gene or loci agnostic fashion."}

    LitCovid-sentences

    {"project":"LitCovid-sentences","denotations":[{"id":"T300","span":{"begin":0,"end":34},"obj":"Sentence"},{"id":"T301","span":{"begin":35,"end":166},"obj":"Sentence"},{"id":"T302","span":{"begin":167,"end":340},"obj":"Sentence"},{"id":"T303","span":{"begin":341,"end":514},"obj":"Sentence"},{"id":"T304","span":{"begin":515,"end":735},"obj":"Sentence"},{"id":"T305","span":{"begin":736,"end":1023},"obj":"Sentence"},{"id":"T306","span":{"begin":1024,"end":1276},"obj":"Sentence"},{"id":"T307","span":{"begin":1277,"end":1553},"obj":"Sentence"},{"id":"T308","span":{"begin":1554,"end":1838},"obj":"Sentence"},{"id":"T309","span":{"begin":1839,"end":2073},"obj":"Sentence"},{"id":"T310","span":{"begin":2074,"end":2268},"obj":"Sentence"},{"id":"T311","span":{"begin":2269,"end":2533},"obj":"Sentence"},{"id":"T312","span":{"begin":2534,"end":2679},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Susceptibility and Risk Biomarkers\nThere are currently limited known risk factors for susceptibility to COVID-19, although this has been evaluated in several studies. Zhao et al. compared the ABO blood group distribution in a cohort of 2,173 COVID-19 patients to that of healthy controls from the corresponding regions (Zhao et al., 2020b). They found blood group A to be associated with a higher risk for acquiring COVID-19 when compared to non-A blood groups; blood group O had the lowest risk for the infection. Another study demonstrated an identical association (Zietz and Tatonetti, 2020), and similar results have been previously described for other viruses (Lindesmith et al., 2003), including SARS-CoV-1 (Cheng et al., 2005a).\nSeveral large collaborative efforts are currently underway to generate, share, and analyze genetic data to understand the links between human genetic variation and COVID-19 susceptibility and severity, the most prominent of which is the COVID-19 Host Genetics Initiative (covid19hg.org). These studies are supported by previous observations on SARS-CoV-1 that followed the 2003 outbreak, which have identified significant associations between genetic variants and immune phenotypes (Chan et al., 2007, Wang et al., 2011, Zhao et al., 2011). Although identifying such polymorphisms and their associated genes and pathways for SARS-CoV-2 will require large cohorts, several studies, which remain to be tested in clinical trials, have already highlighted genetic polymorphisms that may potentially impact susceptibility. These studies have focused on genetic variants that may impact the expression or function of genes important in viral entry, namely ACE2 (SARS-CoV-2 receptor) and TMPRSS2 (spike protein activator) (Asselta et al., 2020, Cao et al., 2020c, Renieri et al., 2020, Stawiski et al., 2020). Cao et al. identified variants that are potentially expression quantitative trait loci (eQTL) of ACE2 (i.e., they may potentially alter ACE2 gene expression) and analyzed their frequencies in different populations (Cao et al., 2020c). Stawiski et al. listed variants that may be critical in ACE2 binding and thereby its function and compared the frequencies of these variants within different populations (Stawiski et al., 2020).\nWhile there are several limitations to these studies, the major question is whether the utility of these biomarkers is replicable in large populations with COVID-19 clinical outcomes data and in targeted or large-scale genomic analyses that are currently underway. In addition, these studies will reveal the potential associations between genetic variants and susceptibility in a gene or loci agnostic fashion."}