CovidStanfordV1, Main, Exploration, bibRecord, 000330

Reduced development of COVID-19 in children reveals molecular checkpoints gating pathogenesis illuminating potential therapeutics.

Identifieur interne : 000330 ( Main/Exploration ); précédent : 000329; suivant : 000331

Reduced development of COVID-19 in children reveals molecular checkpoints gating pathogenesis illuminating potential therapeutics.

Auteurs : Jonathan Baruch Steinman [États-Unis] ; Fok Moon Lum [États-Unis] ; Peggy Pui-Kay Ho [États-Unis] ; Naftali Kaminski [États-Unis] ; Lawrence Steinman [États-Unis]

Source :

Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2020.

RBID : pubmed:32883878

Descripteurs français

English descriptors

KwdEn :
- Angiotensin-Converting Enzyme 2 (MeSH), Betacoronavirus (metabolism), COVID-19 (MeSH), Child (MeSH), Coronavirus Infections (immunology), Coronavirus Infections (metabolism), Coronavirus Infections (virology), Host-Pathogen Interactions (immunology), Humans (MeSH), Pandemics (MeSH), Peptidyl-Dipeptidase A (metabolism), Pneumonia, Viral (immunology), Pneumonia, Viral (metabolism), Pneumonia, Viral (virology), Respiratory Mucosa (metabolism), Respiratory Tract Infections (immunology), Respiratory Tract Infections (virology), SARS-CoV-2 (MeSH), Th2 Cells (physiology).
MESH :
- chemical , metabolism : Peptidyl-Dipeptidase A.
- chemical : Angiotensin-Converting Enzyme 2.
- immunology : Coronavirus Infections, Host-Pathogen Interactions, Pneumonia, Viral, Respiratory Tract Infections.
- metabolism : Betacoronavirus, Coronavirus Infections, Pneumonia, Viral, Respiratory Mucosa.
- physiology : Th2 Cells.
- virology : Coronavirus Infections, Pneumonia, Viral, Respiratory Tract Infections.
- COVID-19, Child, Humans, Pandemics, SARS-CoV-2.

Abstract

The reduced development of COVID-19 for children compared to adults provides some tantalizing clues on the pathogenesis and transmissibility of this pandemic virus. First, ACE2, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) receptor, is reduced in the respiratory tract in children. Second, coronavirus associated with common colds in children may offer some protection, due to cross-reactive humoral immunity and T cell immunity between common coronaviruses and SARS-CoV-2. Third, T helper 2 immune responses are protective in children. Fourth, surprisingly, eosinophilia, associated with T helper 2, may be protective. Fifth, children generally produce lower levels of inflammatory cytokines. Finally, the influence of the downturn in the global economy, the impact of living in quarters among families who are the most at risk, and factors including the openings of some schools, are considered. Those most disadvantaged socioeconomically may suffer disproportionately with COVID-19.

DOI: 10.1073/pnas.2012358117
PubMed: 32883878
PubMed Central: PMC7547272

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000352
to stream Main, to step Curation: 000352

Le document en format XML

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<term>COVID-19 (MeSH)</term>
<term>Child (MeSH)</term>
<term>Coronavirus Infections (immunology)</term>
<term>Coronavirus Infections (metabolism)</term>
<term>Coronavirus Infections (virology)</term>
<term>Host-Pathogen Interactions (immunology)</term>
<term>Humans (MeSH)</term>
<term>Pandemics (MeSH)</term>
<term>Peptidyl-Dipeptidase A (metabolism)</term>
<term>Pneumonia, Viral (immunology)</term>
<term>Pneumonia, Viral (metabolism)</term>
<term>Pneumonia, Viral (virology)</term>
<term>Respiratory Mucosa (metabolism)</term>
<term>Respiratory Tract Infections (immunology)</term>
<term>Respiratory Tract Infections (virology)</term>
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<term>Th2 Cells (physiology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Betacoronavirus (métabolisme)</term>
<term>Enfant (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Infections de l'appareil respiratoire (immunologie)</term>
<term>Infections de l'appareil respiratoire (virologie)</term>
<term>Infections à coronavirus (immunologie)</term>
<term>Infections à coronavirus (métabolisme)</term>
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<term>Interactions hôte-pathogène (immunologie)</term>
<term>Lymphocytes auxiliaires Th2 (physiologie)</term>
<term>Muqueuse respiratoire (métabolisme)</term>
<term>Pandémies (MeSH)</term>
<term>Peptidyl-Dipeptidase A (métabolisme)</term>
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<term>Pneumopathie virale (métabolisme)</term>
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<term>Infections à coronavirus</term>
<term>Interactions hôte-pathogène</term>
<term>Pneumopathie virale</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Coronavirus Infections</term>
<term>Host-Pathogen Interactions</term>
<term>Pneumonia, Viral</term>
<term>Respiratory Tract Infections</term>
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<term>Coronavirus Infections</term>
<term>Pneumonia, Viral</term>
<term>Respiratory Mucosa</term>
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<term>Infections à coronavirus</term>
<term>Muqueuse respiratoire</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Pneumopathie virale</term>
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<front><div type="abstract" xml:lang="en">The reduced development of COVID-19 for children compared to adults provides some tantalizing clues on the pathogenesis and transmissibility of this pandemic virus. First, ACE2, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) receptor, is reduced in the respiratory tract in children. Second, coronavirus associated with common colds in children may offer some protection, due to cross-reactive humoral immunity and T cell immunity between common coronaviruses and SARS-CoV-2. Third, T helper 2 immune responses are protective in children. Fourth, surprisingly, eosinophilia, associated with T helper 2, may be protective. Fifth, children generally produce lower levels of inflammatory cytokines. Finally, the influence of the downturn in the global economy, the impact of living in quarters among families who are the most at risk, and factors including the openings of some schools, are considered. Those most disadvantaged socioeconomically may suffer disproportionately with COVID-19.</div>
</front>
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<Month>10</Month>
<Day>19</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>12</Month>
<Day>18</Day>
</DateRevised>
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<JournalIssue CitedMedium="Internet"><Volume>117</Volume>
<Issue>40</Issue>
<PubDate><Year>2020</Year>
<Month>10</Month>
<Day>06</Day>
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<Title>Proceedings of the National Academy of Sciences of the United States of America</Title>
<ISOAbbreviation>Proc Natl Acad Sci U S A</ISOAbbreviation>
</Journal>
<ArticleTitle>Reduced development of COVID-19 in children reveals molecular checkpoints gating pathogenesis illuminating potential therapeutics.</ArticleTitle>
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<Abstract><AbstractText>The reduced development of COVID-19 for children compared to adults provides some tantalizing clues on the pathogenesis and transmissibility of this pandemic virus. First, ACE2, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) receptor, is reduced in the respiratory tract in children. Second, coronavirus associated with common colds in children may offer some protection, due to cross-reactive humoral immunity and T cell immunity between common coronaviruses and SARS-CoV-2. Third, T helper 2 immune responses are protective in children. Fourth, surprisingly, eosinophilia, associated with T helper 2, may be protective. Fifth, children generally produce lower levels of inflammatory cytokines. Finally, the influence of the downturn in the global economy, the impact of living in quarters among families who are the most at risk, and factors including the openings of some schools, are considered. Those most disadvantaged socioeconomically may suffer disproportionately with COVID-19.</AbstractText>
<CopyrightInformation>Copyright © 2020 the Author(s). Published by PNAS.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Steinman</LastName>
<ForeName>Jonathan Baruch</ForeName>
<Initials>JB</Initials>
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<AffiliationInfo><Affiliation>Department of Pediatrics, Columbia University, New York, NY 10032.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lum</LastName>
<ForeName>Fok Moon</ForeName>
<Initials>FM</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, Stanford University, Stanford CA 94305.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Neurology & Neurological Sciences, Stanford University, Stanford, CA 94305.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Ho</LastName>
<ForeName>Peggy Pui-Kay</ForeName>
<Initials>PP</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, Stanford University, Stanford CA 94305.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Neurology & Neurological Sciences, Stanford University, Stanford, CA 94305.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kaminski</LastName>
<ForeName>Naftali</ForeName>
<Initials>N</Initials>
<Identifier Source="ORCID">0000-0001-5917-4601</Identifier>
<AffiliationInfo><Affiliation>Pulmonary, Critical Care and Sleep Medicine, Yale University School of Medicine, New Haven, CT 06520.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Steinman</LastName>
<ForeName>Lawrence</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, Stanford University, Stanford CA 94305; steinman@stanford.edu.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Neurology & Neurological Sciences, Stanford University, Stanford, CA 94305.</Affiliation>
</AffiliationInfo>
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<Language>eng</Language>
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<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D016454">Review</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2020</Year>
<Month>09</Month>
<Day>03</Day>
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<ISSNLinking>0027-8424</ISSNLinking>
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<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>
</ChemicalList>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000085962" MajorTopicYN="N">Angiotensin-Converting Enzyme 2</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000073640" MajorTopicYN="N">Betacoronavirus</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="N">COVID-19</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054884" MajorTopicYN="N">Host-Pathogen Interactions</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</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="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011024" MajorTopicYN="N">Pneumonia, Viral</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020545" MajorTopicYN="N">Respiratory Mucosa</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012141" MajorTopicYN="N">Respiratory Tract Infections</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000086402" MajorTopicYN="N">SARS-CoV-2</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018418" MajorTopicYN="N">Th2 Cells</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">ACE2</Keyword>
<Keyword MajorTopicYN="Y">COVID-19</Keyword>
<Keyword MajorTopicYN="Y">SARS-CoV-2</Keyword>
<Keyword MajorTopicYN="Y">children</Keyword>
</KeywordList>
<CoiStatement>Competing interest statement: N.K. has consulted with Biogen Idec, Boehringer Ingelheim, Third Rock, Pliant, Samumed, NuMedii, Indaloo, Theravance, LifeMax, Three Lake Partners, RohBar, and reports a grant from Veracyte. N.K. has patents on New Therapies in Pulmonary Fibrosis and Peripheral Blood Gene Expression Biomarkers. All these consultations are outside of this work. L.S. has consulted with Roche, Novartis, Tolerion, Atreca, TG Therapeutics, and Atara Biopharma. All these consultations are outside of the scope of this work.</CoiStatement>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2020</Year>
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Reduced development of COVID-19 in children reveals molecular checkpoints gating pathogenesis illuminating potential therapeutics.

Reduced development of COVID-19 in children reveals molecular checkpoints gating pathogenesis illuminating potential therapeutics.

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