Do genetic polymorphisms in angiotensin converting enzyme 2 (ACE2) gene play a role in coronavirus disease 2019 (COVID-19)?
Identifieur interne : 000612 ( Main/Exploration ); précédent : 000611; suivant : 000613Do genetic polymorphisms in angiotensin converting enzyme 2 (ACE2) gene play a role in coronavirus disease 2019 (COVID-19)?
Auteurs : Giuseppe Lippi [Italie] ; Carl J. Lavie [États-Unis] ; Brandon M. Henry [États-Unis] ; Fabian Sanchis-Gomar [Espagne, États-Unis]Source :
- Clinical chemistry and laboratory medicine [ 1437-4331 ] ; 2020.
Descripteurs français
- KwdFr :
- Betacoronavirus (physiologie), Domaines protéiques (MeSH), Glycoprotéine de spicule des coronavirus (métabolisme), Humains (MeSH), Infections à coronavirus (physiopathologie), Liaison aux protéines (MeSH), Pandémies (MeSH), Peptidyl-Dipeptidase A (composition chimique), Peptidyl-Dipeptidase A (génétique), Peptidyl-Dipeptidase A (métabolisme), Pneumopathie virale (physiopathologie), Polymorphisme génétique (MeSH), Récepteurs viraux (composition chimique), Récepteurs viraux (génétique), Récepteurs viraux (métabolisme).
- MESH :
- composition chimique : Peptidyl-Dipeptidase A, Récepteurs viraux.
- génétique : Peptidyl-Dipeptidase A, Récepteurs viraux.
- métabolisme : Glycoprotéine de spicule des coronavirus, Peptidyl-Dipeptidase A, Récepteurs viraux.
- physiologie : Betacoronavirus.
- physiopathologie : Infections à coronavirus, Pneumopathie virale.
- Domaines protéiques, Humains, Liaison aux protéines, Pandémies, Polymorphisme génétique.
English descriptors
- KwdEn :
- Angiotensin-Converting Enzyme 2 (MeSH), Betacoronavirus (physiology), COVID-19 (MeSH), Coronavirus Infections (physiopathology), Humans (MeSH), Pandemics (MeSH), Peptidyl-Dipeptidase A (chemistry), Peptidyl-Dipeptidase A (genetics), Peptidyl-Dipeptidase A (metabolism), Pneumonia, Viral (physiopathology), Polymorphism, Genetic (MeSH), Protein Binding (MeSH), Protein Domains (MeSH), Receptors, Virus (chemistry), Receptors, Virus (genetics), Receptors, Virus (metabolism), SARS-CoV-2 (MeSH), Spike Glycoprotein, Coronavirus (metabolism).
- MESH :
- chemical , chemistry : Peptidyl-Dipeptidase A, Receptors, Virus.
- chemical , genetics : Peptidyl-Dipeptidase A, Receptors, Virus.
- chemical , metabolism : Peptidyl-Dipeptidase A, Receptors, Virus, Spike Glycoprotein, Coronavirus.
- chemical : Angiotensin-Converting Enzyme 2.
- physiology : Betacoronavirus.
- physiopathology : Coronavirus Infections, Pneumonia, Viral.
- COVID-19, Humans, Pandemics, Polymorphism, Genetic, Protein Binding, Protein Domains, SARS-CoV-2.
Abstract
Although some demographic, clinical and environmental factors have been associated with a higher risk of developing coronavirus disease 2019 (COVID-19) and progressing towards severe disease, altogether these variables do not completely account for the different clinical presentations observed in patients with comparable baseline risk, whereby some subjects may remain totally asymptomatic, whilst others develop a very aggressive illness. Some predisposing genetic backgrounds can hence potentially explain the broad inter-individual variation of disease susceptibility and/or severity. It has been now clearly established that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus causing COVID-19, infects the host cell through biding and being internalized with angiotensin converting enzyme 2 (ACE2), a surface protein expressed in a noticeable number of human cells, especially in those of upper and lower respiratory tracts, heart, kidney, testis, adipose tissue, gastrointestinal system and in lymphocytes. Accumulating evidence now suggests that genetic polymorphisms in the ACE2 gene may modulate intermolecular interactions with the spike protein of SARS-CoV-2 and/or contribute to pulmonary and systemic injury by fostering vasoconstriction, inflammation, oxidation and fibrosis. We hence argue that the development of genetic tests aimed at specifically identifying specific COVID-19-susceptible or -protective ACE2 variants in the general population may be a reasonable strategy for stratifying the risk of infection and/or unfavorable disease progression.
DOI: 10.1515/cclm-2020-0727
PubMed: 32598305
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Lavie</name><affiliation wicri:level="2"><nlm:affiliation>John Ochsner Heart and Vascular Institute, Ochsner Clinical School, The University of Queensland School of Medicine, New Orleans, LA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>John Ochsner Heart and Vascular Institute, Ochsner Clinical School, The University of Queensland School of Medicine, New Orleans, LA</wicri:regionArea><placeName><region type="state">Louisiane</region></placeName></affiliation></author><author><name sortKey="Henry, Brandon M" sort="Henry, Brandon M" uniqKey="Henry B" first="Brandon M" last="Henry">Brandon M. Henry</name><affiliation wicri:level="2"><nlm:affiliation>Cardiac Intensive Care Unit, The Heart Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Cardiac Intensive Care Unit, The Heart Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH</wicri:regionArea><placeName><region type="state">Ohio</region></placeName></affiliation></author><author><name sortKey="Sanchis Gomar, Fabian" sort="Sanchis Gomar, Fabian" uniqKey="Sanchis Gomar F" first="Fabian" last="Sanchis-Gomar">Fabian Sanchis-Gomar</name><affiliation wicri:level="1"><nlm:affiliation>Department of Physiology, Faculty of Medicine, University of Valencia and INCLIVA Biomedical Research Institute, Valencia, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Department of Physiology, Faculty of Medicine, University of Valencia and INCLIVA Biomedical Research Institute, Valencia</wicri:regionArea><wicri:noRegion>Valencia</wicri:noRegion></affiliation><affiliation wicri:level="2"><nlm:affiliation>Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author></analytic><series><title level="j">Clinical chemistry and laboratory medicine</title><idno type="eISSN">1437-4331</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Angiotensin-Converting Enzyme 2 (MeSH)</term><term>Betacoronavirus (physiology)</term><term>COVID-19 (MeSH)</term><term>Coronavirus Infections (physiopathology)</term><term>Humans (MeSH)</term><term>Pandemics (MeSH)</term><term>Peptidyl-Dipeptidase A (chemistry)</term><term>Peptidyl-Dipeptidase A (genetics)</term><term>Peptidyl-Dipeptidase A (metabolism)</term><term>Pneumonia, Viral (physiopathology)</term><term>Polymorphism, Genetic (MeSH)</term><term>Protein Binding (MeSH)</term><term>Protein Domains (MeSH)</term><term>Receptors, Virus (chemistry)</term><term>Receptors, Virus (genetics)</term><term>Receptors, Virus (metabolism)</term><term>SARS-CoV-2 (MeSH)</term><term>Spike Glycoprotein, Coronavirus (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Betacoronavirus (physiologie)</term><term>Domaines protéiques (MeSH)</term><term>Glycoprotéine de spicule des coronavirus (métabolisme)</term><term>Humains (MeSH)</term><term>Infections à coronavirus (physiopathologie)</term><term>Liaison aux protéines (MeSH)</term><term>Pandémies (MeSH)</term><term>Peptidyl-Dipeptidase A (composition chimique)</term><term>Peptidyl-Dipeptidase A (génétique)</term><term>Peptidyl-Dipeptidase A (métabolisme)</term><term>Pneumopathie virale (physiopathologie)</term><term>Polymorphisme génétique (MeSH)</term><term>Récepteurs viraux (composition chimique)</term><term>Récepteurs viraux (génétique)</term><term>Récepteurs viraux (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Peptidyl-Dipeptidase A</term><term>Receptors, Virus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Peptidyl-Dipeptidase A</term><term>Receptors, Virus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Peptidyl-Dipeptidase A</term><term>Receptors, Virus</term><term>Spike Glycoprotein, Coronavirus</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Angiotensin-Converting Enzyme 2</term></keywords><keywords scheme="MESH" qualifier="composition chimique" 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xml:lang="en"><term>COVID-19</term><term>Humans</term><term>Pandemics</term><term>Polymorphism, Genetic</term><term>Protein Binding</term><term>Protein Domains</term><term>SARS-CoV-2</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Domaines protéiques</term><term>Humains</term><term>Liaison aux protéines</term><term>Pandémies</term><term>Polymorphisme génétique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although some demographic, clinical and environmental factors have been associated with a higher risk of developing coronavirus disease 2019 (COVID-19) and progressing towards severe disease, altogether these variables do not completely account for the different clinical presentations observed in patients with comparable baseline risk, whereby some subjects may remain totally asymptomatic, whilst others develop a very aggressive illness. Some predisposing genetic backgrounds can hence potentially explain the broad inter-individual variation of disease susceptibility and/or severity. It has been now clearly established that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus causing COVID-19, infects the host cell through biding and being internalized with angiotensin converting enzyme 2 (ACE2), a surface protein expressed in a noticeable number of human cells, especially in those of upper and lower respiratory tracts, heart, kidney, testis, adipose tissue, gastrointestinal system and in lymphocytes. Accumulating evidence now suggests that genetic polymorphisms in the ACE2 gene may modulate intermolecular interactions with the spike protein of SARS-CoV-2 and/or contribute to pulmonary and systemic injury by fostering vasoconstriction, inflammation, oxidation and fibrosis. We hence argue that the development of genetic tests aimed at specifically identifying specific COVID-19-susceptible or -protective ACE2 variants in the general population may be a reasonable strategy for stratifying the risk of infection and/or unfavorable disease progression.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32598305</PMID><DateCompleted><Year>2020</Year><Month>09</Month><Day>28</Day></DateCompleted><DateRevised><Year>2020</Year><Month>12</Month><Day>18</Day></DateRevised><Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">1437-4331</ISSN><JournalIssue CitedMedium="Internet"><Volume>58</Volume><Issue>9</Issue><PubDate><Year>2020</Year><Month>08</Month><Day>27</Day></PubDate></JournalIssue><Title>Clinical chemistry and laboratory medicine</Title><ISOAbbreviation>Clin Chem Lab Med</ISOAbbreviation></Journal><ArticleTitle>Do genetic polymorphisms in angiotensin converting enzyme 2 (ACE2) gene play a role in coronavirus disease 2019 (COVID-19)?</ArticleTitle><Pagination><MedlinePgn>1415-1422</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1515/cclm-2020-0727</ELocationID><ELocationID EIdType="pii" ValidYN="Y">/j/cclm.2020.58.issue-9/cclm-2020-0727/cclm-2020-0727.xml</ELocationID><Abstract><AbstractText>Although some demographic, clinical and environmental factors have been associated with a higher risk of developing coronavirus disease 2019 (COVID-19) and progressing towards severe disease, altogether these variables do not completely account for the different clinical presentations observed in patients with comparable baseline risk, whereby some subjects may remain totally asymptomatic, whilst others develop a very aggressive illness. Some predisposing genetic backgrounds can hence potentially explain the broad inter-individual variation of disease susceptibility and/or severity. It has been now clearly established that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus causing COVID-19, infects the host cell through biding and being internalized with angiotensin converting enzyme 2 (ACE2), a surface protein expressed in a noticeable number of human cells, especially in those of upper and lower respiratory tracts, heart, kidney, testis, adipose tissue, gastrointestinal system and in lymphocytes. Accumulating evidence now suggests that genetic polymorphisms in the ACE2 gene may modulate intermolecular interactions with the spike protein of SARS-CoV-2 and/or contribute to pulmonary and systemic injury by fostering vasoconstriction, inflammation, oxidation and fibrosis. We hence argue that the development of genetic tests aimed at specifically identifying specific COVID-19-susceptible or -protective ACE2 variants in the general population may be a reasonable strategy for stratifying the risk of infection and/or unfavorable disease progression.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lippi</LastName><ForeName>Giuseppe</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Section of Clinical Biochemistry, Verona, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lavie</LastName><ForeName>Carl J</ForeName><Initials>CJ</Initials><AffiliationInfo><Affiliation>John Ochsner Heart and Vascular Institute, Ochsner Clinical School, The University of Queensland School of Medicine, New Orleans, LA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Henry</LastName><ForeName>Brandon M</ForeName><Initials>BM</Initials><AffiliationInfo><Affiliation>Cardiac Intensive Care Unit, The Heart Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sanchis-Gomar</LastName><ForeName>Fabian</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Physiology, Faculty of Medicine, University of Valencia and INCLIVA Biomedical Research Institute, Valencia, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>06</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Clin Chem Lab Med</MedlineTA><NlmUniqueID>9806306</NlmUniqueID><ISSNLinking>1434-6621</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011991">Receptors, Virus</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D064370">Spike Glycoprotein, Coronavirus</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C000657845">spike protein, SARS-CoV-2</NameOfSubstance></Chemical><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></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000085962" MajorTopicYN="N">Angiotensin-Converting Enzyme 2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000073640" MajorTopicYN="N">Betacoronavirus</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="N">COVID-19</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058873" MajorTopicYN="N">Pandemics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007703" MajorTopicYN="N">Peptidyl-Dipeptidase A</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011024" MajorTopicYN="N">Pneumonia, Viral</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011110" MajorTopicYN="Y">Polymorphism, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011485" MajorTopicYN="N">Protein Binding</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000072417" MajorTopicYN="N">Protein Domains</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011991" MajorTopicYN="N">Receptors, Virus</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000086402" MajorTopicYN="N">SARS-CoV-2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D064370" MajorTopicYN="N">Spike Glycoprotein, Coronavirus</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">COVID-19</Keyword><Keyword MajorTopicYN="Y">angiotensin</Keyword><Keyword MajorTopicYN="Y">enzyme</Keyword><Keyword MajorTopicYN="Y">polymorphism</Keyword><Keyword MajorTopicYN="Y">receptor</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>05</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>05</Month><Day>28</Day></PubMedPubDate><PubMedPubDate 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Lippi</name></noRegion></country><country name="États-Unis"><region name="Louisiane"><name sortKey="Lavie, Carl J" sort="Lavie, Carl J" uniqKey="Lavie C" first="Carl J" last="Lavie">Carl J. Lavie</name></region><name sortKey="Henry, Brandon M" sort="Henry, Brandon M" uniqKey="Henry B" first="Brandon M" last="Henry">Brandon M. Henry</name><name sortKey="Sanchis Gomar, Fabian" sort="Sanchis Gomar, Fabian" uniqKey="Sanchis Gomar F" first="Fabian" last="Sanchis-Gomar">Fabian Sanchis-Gomar</name></country><country name="Espagne"><noRegion><name sortKey="Sanchis Gomar, Fabian" sort="Sanchis Gomar, Fabian" uniqKey="Sanchis Gomar F" first="Fabian" last="Sanchis-Gomar">Fabian Sanchis-Gomar</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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