New insights into genetic susceptibility of COVID-19: an ACE2 and TMPRSS2 polymorphism analysis.
Identifieur interne : 001151 ( Main/Curation ); précédent : 001150; suivant : 001152New insights into genetic susceptibility of COVID-19: an ACE2 and TMPRSS2 polymorphism analysis.
Auteurs : Yuan Hou [États-Unis] ; Junfei Zhao [États-Unis] ; William Martin [États-Unis] ; Asha Kallianpur [États-Unis] ; Mina K. Chung [États-Unis] ; Lara Jehi [États-Unis] ; Nima Sharifi [États-Unis] ; Serpil Erzurum [États-Unis] ; Charis Eng [États-Unis] ; Feixiong Cheng [États-Unis]Source :
- BMC medicine [ 1741-7015 ] ; 2020.
Descripteurs français
- KwdFr :
- Betacoronavirus (MeSH), Facteurs de risque (MeSH), Génétique des populations (MeSH), Humains (MeSH), Infections à coronavirus (ethnologie), Infections à coronavirus (génétique), Locus de caractère quantitatif (MeSH), Mâle (MeSH), Pandémies (MeSH), Peptidyl-Dipeptidase A (génétique), Pneumopathie virale (ethnologie), Pneumopathie virale (génétique), Polymorphisme génétique (MeSH), Population d'origine africaine (MeSH), Prédisposition génétique à une maladie (MeSH), Serine endopeptidases (génétique).
- MESH :
- ethnologie : Infections à coronavirus, Pneumopathie virale.
- génétique : Infections à coronavirus, Peptidyl-Dipeptidase A, Pneumopathie virale, Serine endopeptidases.
- Betacoronavirus, Facteurs de risque, Génétique des populations, Humains, Locus de caractère quantitatif, Mâle, Pandémies, Polymorphisme génétique, Population d'origine africaine, Prédisposition génétique à une maladie.
English descriptors
- KwdEn :
- African Continental Ancestry Group (MeSH), Angiotensin-Converting Enzyme 2 (MeSH), Betacoronavirus (MeSH), COVID-19 (MeSH), Coronavirus Infections (ethnology), Coronavirus Infections (genetics), Genetic Predisposition to Disease (MeSH), Genetics, Population (MeSH), Humans (MeSH), Male (MeSH), Pandemics (MeSH), Peptidyl-Dipeptidase A (genetics), Pneumonia, Viral (ethnology), Pneumonia, Viral (genetics), Polymorphism, Genetic (MeSH), Quantitative Trait Loci (MeSH), Risk Factors (MeSH), SARS-CoV-2 (MeSH), Serine Endopeptidases (genetics).
- MESH :
- chemical , genetics : Peptidyl-Dipeptidase A, Serine Endopeptidases.
- chemical : Angiotensin-Converting Enzyme 2.
- ethnology : Coronavirus Infections, Pneumonia, Viral.
- genetics : Coronavirus Infections, Pneumonia, Viral.
- African Continental Ancestry Group, Betacoronavirus, COVID-19, Genetic Predisposition to Disease, Genetics, Population, Humans, Male, Pandemics, Polymorphism, Genetic, Quantitative Trait Loci, Risk Factors, SARS-CoV-2.
Abstract
BACKGROUND
Coronavirus Disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has now been confirmed worldwide. Yet, COVID-19 is strangely and tragically selective. Morbidity and mortality due to COVID19 rise dramatically with age and co-existing health conditions, including cancer and cardiovascular diseases. Human genetic factors may contribute to the extremely high transmissibility of SARS-CoV-2 and to the relentlessly progressive disease observed in a small but significant proportion of infected individuals, but these factors are largely unknown.
MAIN BODY
In this study, we investigated genetic susceptibility to COVID-19 by examining DNA polymorphisms in ACE2 and TMPRSS2 (two key host factors of SARS-CoV-2) from ~ 81,000 human genomes. We found unique genetic susceptibility across different populations in ACE2 and TMPRSS2. Specifically, ACE2 polymorphisms were found to be associated with cardiovascular and pulmonary conditions by altering the angiotensinogen-ACE2 interactions, such as p.Arg514Gly in the African/African-American population. Unique but prevalent polymorphisms (including p.Val160Met (rs12329760), an expression quantitative trait locus (eQTL)) in TMPRSS2, offer potential explanations for differential genetic susceptibility to COVID-19 as well as for risk factors, including those with cancer and the high-risk group of male patients. We further discussed that polymorphisms in ACE2 or TMPRSS2 could guide effective treatments (i.e., hydroxychloroquine and camostat) for COVID-19.
CONCLUSION
This study suggested that ACE2 or TMPRSS2 DNA polymorphisms were likely associated with genetic susceptibility of COVID-19, which calls for a human genetics initiative for fighting the COVID-19 pandemic.
DOI: 10.1186/s12916-020-01673-z
PubMed: 32664879
PubMed Central: PMC7360473
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<author><name sortKey="Jehi, Lara" sort="Jehi, Lara" uniqKey="Jehi L" first="Lara" last="Jehi">Lara Jehi</name>
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<author><name sortKey="Sharifi, Nima" sort="Sharifi, Nima" uniqKey="Sharifi N" first="Nima" last="Sharifi">Nima Sharifi</name>
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<author><name sortKey="Erzurum, Serpil" sort="Erzurum, Serpil" uniqKey="Erzurum S" first="Serpil" last="Erzurum">Serpil Erzurum</name>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Eng, Charis" sort="Eng, Charis" uniqKey="Eng C" first="Charis" last="Eng">Charis Eng</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>African Continental Ancestry Group (MeSH)</term>
<term>Angiotensin-Converting Enzyme 2 (MeSH)</term>
<term>Betacoronavirus (MeSH)</term>
<term>COVID-19 (MeSH)</term>
<term>Coronavirus Infections (ethnology)</term>
<term>Coronavirus Infections (genetics)</term>
<term>Genetic Predisposition to Disease (MeSH)</term>
<term>Genetics, Population (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Male (MeSH)</term>
<term>Pandemics (MeSH)</term>
<term>Peptidyl-Dipeptidase A (genetics)</term>
<term>Pneumonia, Viral (ethnology)</term>
<term>Pneumonia, Viral (genetics)</term>
<term>Polymorphism, Genetic (MeSH)</term>
<term>Quantitative Trait Loci (MeSH)</term>
<term>Risk Factors (MeSH)</term>
<term>SARS-CoV-2 (MeSH)</term>
<term>Serine Endopeptidases (genetics)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Betacoronavirus (MeSH)</term>
<term>Facteurs de risque (MeSH)</term>
<term>Génétique des populations (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Infections à coronavirus (ethnologie)</term>
<term>Infections à coronavirus (génétique)</term>
<term>Locus de caractère quantitatif (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Pandémies (MeSH)</term>
<term>Peptidyl-Dipeptidase A (génétique)</term>
<term>Pneumopathie virale (ethnologie)</term>
<term>Pneumopathie virale (génétique)</term>
<term>Polymorphisme génétique (MeSH)</term>
<term>Population d'origine africaine (MeSH)</term>
<term>Prédisposition génétique à une maladie (MeSH)</term>
<term>Serine endopeptidases (génétique)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Peptidyl-Dipeptidase A</term>
<term>Serine Endopeptidases</term>
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<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Angiotensin-Converting Enzyme 2</term>
</keywords>
<keywords scheme="MESH" qualifier="ethnologie" xml:lang="fr"><term>Infections à coronavirus</term>
<term>Pneumopathie virale</term>
</keywords>
<keywords scheme="MESH" qualifier="ethnology" xml:lang="en"><term>Coronavirus Infections</term>
<term>Pneumonia, Viral</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Coronavirus Infections</term>
<term>Pneumonia, Viral</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Infections à coronavirus</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Pneumopathie virale</term>
<term>Serine endopeptidases</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>African Continental Ancestry Group</term>
<term>Betacoronavirus</term>
<term>COVID-19</term>
<term>Genetic Predisposition to Disease</term>
<term>Genetics, Population</term>
<term>Humans</term>
<term>Male</term>
<term>Pandemics</term>
<term>Polymorphism, Genetic</term>
<term>Quantitative Trait Loci</term>
<term>Risk Factors</term>
<term>SARS-CoV-2</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Betacoronavirus</term>
<term>Facteurs de risque</term>
<term>Génétique des populations</term>
<term>Humains</term>
<term>Locus de caractère quantitatif</term>
<term>Mâle</term>
<term>Pandémies</term>
<term>Polymorphisme génétique</term>
<term>Population d'origine africaine</term>
<term>Prédisposition génétique à une maladie</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>Coronavirus Disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has now been confirmed worldwide. Yet, COVID-19 is strangely and tragically selective. Morbidity and mortality due to COVID19 rise dramatically with age and co-existing health conditions, including cancer and cardiovascular diseases. Human genetic factors may contribute to the extremely high transmissibility of SARS-CoV-2 and to the relentlessly progressive disease observed in a small but significant proportion of infected individuals, but these factors are largely unknown.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>MAIN BODY</b>
</p>
<p>In this study, we investigated genetic susceptibility to COVID-19 by examining DNA polymorphisms in ACE2 and TMPRSS2 (two key host factors of SARS-CoV-2) from ~ 81,000 human genomes. We found unique genetic susceptibility across different populations in ACE2 and TMPRSS2. Specifically, ACE2 polymorphisms were found to be associated with cardiovascular and pulmonary conditions by altering the angiotensinogen-ACE2 interactions, such as p.Arg514Gly in the African/African-American population. Unique but prevalent polymorphisms (including p.Val160Met (rs12329760), an expression quantitative trait locus (eQTL)) in TMPRSS2, offer potential explanations for differential genetic susceptibility to COVID-19 as well as for risk factors, including those with cancer and the high-risk group of male patients. We further discussed that polymorphisms in ACE2 or TMPRSS2 could guide effective treatments (i.e., hydroxychloroquine and camostat) for COVID-19.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSION</b>
</p>
<p>This study suggested that ACE2 or TMPRSS2 DNA polymorphisms were likely associated with genetic susceptibility of COVID-19, which calls for a human genetics initiative for fighting the COVID-19 pandemic.</p>
</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" IndexingMethod="Curated" Owner="NLM"><PMID Version="1">32664879</PMID>
<DateCompleted><Year>2020</Year>
<Month>07</Month>
<Day>21</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>12</Month>
<Day>18</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1741-7015</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>18</Volume>
<Issue>1</Issue>
<PubDate><Year>2020</Year>
<Month>07</Month>
<Day>15</Day>
</PubDate>
</JournalIssue>
<Title>BMC medicine</Title>
<ISOAbbreviation>BMC Med</ISOAbbreviation>
</Journal>
<ArticleTitle>New insights into genetic susceptibility of COVID-19: an ACE2 and TMPRSS2 polymorphism analysis.</ArticleTitle>
<Pagination><MedlinePgn>216</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1186/s12916-020-01673-z</ELocationID>
<Abstract><AbstractText Label="BACKGROUND">Coronavirus Disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has now been confirmed worldwide. Yet, COVID-19 is strangely and tragically selective. Morbidity and mortality due to COVID19 rise dramatically with age and co-existing health conditions, including cancer and cardiovascular diseases. Human genetic factors may contribute to the extremely high transmissibility of SARS-CoV-2 and to the relentlessly progressive disease observed in a small but significant proportion of infected individuals, but these factors are largely unknown.</AbstractText>
<AbstractText Label="MAIN BODY">In this study, we investigated genetic susceptibility to COVID-19 by examining DNA polymorphisms in ACE2 and TMPRSS2 (two key host factors of SARS-CoV-2) from ~ 81,000 human genomes. We found unique genetic susceptibility across different populations in ACE2 and TMPRSS2. Specifically, ACE2 polymorphisms were found to be associated with cardiovascular and pulmonary conditions by altering the angiotensinogen-ACE2 interactions, such as p.Arg514Gly in the African/African-American population. Unique but prevalent polymorphisms (including p.Val160Met (rs12329760), an expression quantitative trait locus (eQTL)) in TMPRSS2, offer potential explanations for differential genetic susceptibility to COVID-19 as well as for risk factors, including those with cancer and the high-risk group of male patients. We further discussed that polymorphisms in ACE2 or TMPRSS2 could guide effective treatments (i.e., hydroxychloroquine and camostat) for COVID-19.</AbstractText>
<AbstractText Label="CONCLUSION">This study suggested that ACE2 or TMPRSS2 DNA polymorphisms were likely associated with genetic susceptibility of COVID-19, which calls for a human genetics initiative for fighting the COVID-19 pandemic.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hou</LastName>
<ForeName>Yuan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhao</LastName>
<ForeName>Junfei</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Systems Biology and Department of Biomedical Informatics, Herbert Irving Comprehensive Center, Columbia University, New York, NY, 10032, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Martin</LastName>
<ForeName>William</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kallianpur</LastName>
<ForeName>Asha</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, 44195, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chung</LastName>
<ForeName>Mina K</ForeName>
<Initials>MK</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, 44195, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Heart, Vascular and Thoracic Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jehi</LastName>
<ForeName>Lara</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sharifi</LastName>
<ForeName>Nima</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, 44195, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Erzurum</LastName>
<ForeName>Serpil</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, 44195, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Eng</LastName>
<ForeName>Charis</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, 44195, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Genetics and Genome Sciences, School of Medicine, Case Western Reserve University, Cleveland, OH, 44106, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Case Comprehensive Cancer Center, School of Medicine, Case Western Reserve University, Cleveland, OH, 44106, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cheng</LastName>
<ForeName>Feixiong</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA. chengf@ccf.org.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, 44195, USA. chengf@ccf.org.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Case Comprehensive Cancer Center, School of Medicine, Case Western Reserve University, Cleveland, OH, 44106, USA. chengf@ccf.org.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R00HL138272</GrantID>
<Agency>Foundation for the National Institutes of Health</Agency>
<Country>International</Country>
</Grant>
<Grant><GrantID>R01AG066707</GrantID>
<Agency>Foundation for the National Institutes of Health</Agency>
<Country>International</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016422">Letter</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2020</Year>
<Month>07</Month>
<Day>15</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>BMC Med</MedlineTA>
<NlmUniqueID>101190723</NlmUniqueID>
<ISSNLinking>1741-7015</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>EC 3.4.15.1</RegistryNumber>
<NameOfSubstance UI="D007703">Peptidyl-Dipeptidase A</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.17.23</RegistryNumber>
<NameOfSubstance UI="C000705307">ACE2 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.17.23</RegistryNumber>
<NameOfSubstance UI="D000085962">Angiotensin-Converting Enzyme 2</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.21.-</RegistryNumber>
<NameOfSubstance UI="D012697">Serine Endopeptidases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.21.-</RegistryNumber>
<NameOfSubstance UI="C421305">TMPRSS2 protein, human</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D044383" MajorTopicYN="N">African Continental Ancestry Group</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000085962" MajorTopicYN="N">Angiotensin-Converting Enzyme 2</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000073640" MajorTopicYN="N">Betacoronavirus</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="N">COVID-19</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName>
<QualifierName UI="Q000208" MajorTopicYN="N">ethnology</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020022" MajorTopicYN="Y">Genetic Predisposition to Disease</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005828" MajorTopicYN="N">Genetics, Population</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058873" MajorTopicYN="N">Pandemics</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007703" MajorTopicYN="N">Peptidyl-Dipeptidase A</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011024" MajorTopicYN="N">Pneumonia, Viral</DescriptorName>
<QualifierName UI="Q000208" MajorTopicYN="N">ethnology</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011110" MajorTopicYN="N">Polymorphism, Genetic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D040641" MajorTopicYN="N">Quantitative Trait Loci</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000086402" MajorTopicYN="N">SARS-CoV-2</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012697" MajorTopicYN="N">Serine Endopeptidases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Angiotensin-converting enzyme 2 (ACE2)</Keyword>
<Keyword MajorTopicYN="Y">COVID-19</Keyword>
<Keyword MajorTopicYN="Y">Coronavirus</Keyword>
<Keyword MajorTopicYN="Y">Genetic susceptibility</Keyword>
<Keyword MajorTopicYN="Y">SARS-CoV-2</Keyword>
<Keyword MajorTopicYN="Y">TMPRSS2</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year>
<Month>04</Month>
<Day>25</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2020</Year>
<Month>06</Month>
<Day>22</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2020</Year>
<Month>7</Month>
<Day>16</Day>
<Hour>6</Hour>
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