PandemieGrippaleV1, PubMed, Checkpoint, bibRecord, 000638

Human Dendritic Cell Response Signatures Distinguish 1918, Pandemic, and Seasonal H1N1 Influenza Viruses.

Identifieur interne : 000638 ( PubMed/Checkpoint ); précédent : 000637; suivant : 000639

Human Dendritic Cell Response Signatures Distinguish 1918, Pandemic, and Seasonal H1N1 Influenza Viruses.

Auteurs : Boris M. Hartmann [États-Unis] ; Juilee Thakar [États-Unis] ; Randy A. Albrecht [États-Unis] ; Stefan Avey [États-Unis] ; Elena Zaslavsky [États-Unis] ; Nada Marjanovic [États-Unis] ; Maria Chikina [États-Unis] ; Miguel Fribourg [États-Unis] ; Fernand Hayot [États-Unis] ; Mirco Schmolke [Suisse] ; Hailong Meng [États-Unis] ; James Wetmur [États-Unis] ; Adolfo García-Sastre [États-Unis] ; Steven H. Kleinstein [États-Unis] ; Stuart C. Sealfon [États-Unis]

Source :

Journal of virology [ 1098-5514 ] ; 2015.

RBID : pubmed:26223639

Descripteurs français

English descriptors

KwdEn :
- Antigenic Variation, Dendritic Cells (immunology), Dendritic Cells (virology), Europe (epidemiology), Gene Expression Profiling, Gene Expression Regulation, History, 20th Century, History, 21st Century, Host-Pathogen Interactions, Humans, Influenza A Virus, H1N1 Subtype (genetics), Influenza A Virus, H1N1 Subtype (immunology), Influenza Pandemic, 1918-1919 (history), Influenza, Human (epidemiology), Influenza, Human (genetics), Influenza, Human (history), Influenza, Human (immunology), Interferons (genetics), Interferons (immunology), Molecular Epidemiology, NF-kappa B (genetics), NF-kappa B (immunology), Pandemics, Reassortant Viruses (genetics), Reassortant Viruses (immunology), Recombination, Genetic, Seasons, Signal Transduction, Time Factors, United States (epidemiology).
MESH :
- chemical , genetics : Interferons, NF-kappa B.
- geographic , epidemiology : Europe, United States.
- epidemiology : Influenza, Human.
- genetics : Influenza A Virus, H1N1 Subtype, Influenza, Human, Reassortant Viruses.
- history : Influenza Pandemic, 1918-1919, Influenza, Human.
- immunology : Dendritic Cells, Influenza A Virus, H1N1 Subtype, Influenza, Human, Interferons, NF-kappa B, Reassortant Viruses.
- virology : Dendritic Cells.
- Antigenic Variation, Gene Expression Profiling, Gene Expression Regulation, History, 20th Century, History, 21st Century, Host-Pathogen Interactions, Humans, Molecular Epidemiology, Pandemics, Recombination, Genetic, Seasons, Signal Transduction, Time Factors.

Abstract

Influenza viruses continue to present global threats to human health. Antigenic drift and shift, genetic reassortment, and cross-species transmission generate new strains with differences in epidemiology and clinical severity. We compared the temporal transcriptional responses of human dendritic cells (DC) to infection with two pandemic (A/Brevig Mission/1/1918, A/California/4/2009) and two seasonal (A/New Caledonia/20/1999, A/Texas/36/1991) H1N1 influenza viruses. Strain-specific response differences included stronger activation of NF-κB following infection with A/New Caledonia/20/1999 and a unique cluster of genes expressed following infection with A/Brevig Mission/1/1918. A common antiviral program showing strain-specific timing was identified in the early DC response and found to correspond with reported transcript changes in blood during symptomatic human influenza virus infection. Comparison of the global responses to the seasonal and pandemic strains showed that a dramatic divergence occurred after 4 h, with only the seasonal strains inducing widespread mRNA loss.

DOI: 10.1128/JVI.01523-15
PubMed: 26223639

Affiliations:

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Le document en format XML

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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Meng, Hailong" sort="Meng, Hailong" uniqKey="Meng H" first="Hailong" last="Meng">Hailong Meng</name>
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<placeName><region type="state">Connecticut</region>
</placeName>
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<author><name sortKey="Sealfon, Stuart C" sort="Sealfon, Stuart C" uniqKey="Sealfon S" first="Stuart C" last="Sealfon">Stuart C. Sealfon</name>
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<wicri:regionArea>Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA Center for Translational Systems Biology, Icahn School of Medicine at Mount Sinai, New York, New York</wicri:regionArea>
<placeName><region type="state">État de New York</region>
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<series><title level="j">Journal of virology</title>
<idno type="eISSN">1098-5514</idno>
<imprint><date when="2015" type="published">2015</date>
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<front><div type="abstract" xml:lang="en">Influenza viruses continue to present global threats to human health. Antigenic drift and shift, genetic reassortment, and cross-species transmission generate new strains with differences in epidemiology and clinical severity. We compared the temporal transcriptional responses of human dendritic cells (DC) to infection with two pandemic (A/Brevig Mission/1/1918, A/California/4/2009) and two seasonal (A/New Caledonia/20/1999, A/Texas/36/1991) H1N1 influenza viruses. Strain-specific response differences included stronger activation of NF-κB following infection with A/New Caledonia/20/1999 and a unique cluster of genes expressed following infection with A/Brevig Mission/1/1918. A common antiviral program showing strain-specific timing was identified in the early DC response and found to correspond with reported transcript changes in blood during symptomatic human influenza virus infection. Comparison of the global responses to the seasonal and pandemic strains showed that a dramatic divergence occurred after 4 h, with only the seasonal strains inducing widespread mRNA loss.</div>
</front>
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<DateCompleted><Year>2015</Year>
<Month>12</Month>
<Day>16</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>03</Month>
<Day>06</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>89</Volume>
<Issue>20</Issue>
<PubDate><Year>2015</Year>
<Month>Oct</Month>
</PubDate>
</JournalIssue>
<Title>Journal of virology</Title>
<ISOAbbreviation>J. Virol.</ISOAbbreviation>
</Journal>
<ArticleTitle>Human Dendritic Cell Response Signatures Distinguish 1918, Pandemic, and Seasonal H1N1 Influenza Viruses.</ArticleTitle>
<Pagination><MedlinePgn>10190-205</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.01523-15</ELocationID>
<Abstract><AbstractText Label="UNLABELLED">Influenza viruses continue to present global threats to human health. Antigenic drift and shift, genetic reassortment, and cross-species transmission generate new strains with differences in epidemiology and clinical severity. We compared the temporal transcriptional responses of human dendritic cells (DC) to infection with two pandemic (A/Brevig Mission/1/1918, A/California/4/2009) and two seasonal (A/New Caledonia/20/1999, A/Texas/36/1991) H1N1 influenza viruses. Strain-specific response differences included stronger activation of NF-κB following infection with A/New Caledonia/20/1999 and a unique cluster of genes expressed following infection with A/Brevig Mission/1/1918. A common antiviral program showing strain-specific timing was identified in the early DC response and found to correspond with reported transcript changes in blood during symptomatic human influenza virus infection. Comparison of the global responses to the seasonal and pandemic strains showed that a dramatic divergence occurred after 4 h, with only the seasonal strains inducing widespread mRNA loss.</AbstractText>
<AbstractText Label="IMPORTANCE" NlmCategory="OBJECTIVE">Continuously evolving influenza viruses present a global threat to human health; however, these host responses display strain-dependent differences that are incompletely understood. Thus, we conducted a detailed comparative study assessing the immune responses of human DC to infection with two pandemic and two seasonal H1N1 influenza strains. We identified in the immune response to viral infection both common and strain-specific features. Among the stain-specific elements were a time shift of the interferon-stimulated gene response, selective induction of NF-κB signaling by one of the seasonal strains, and massive RNA degradation as early as 4 h postinfection by the seasonal, but not the pandemic, viruses. These findings illuminate new aspects of the distinct differences in the immune responses to pandemic and seasonal influenza viruses.</AbstractText>
<CopyrightInformation>Copyright © 2015, American Society for Microbiology. All Rights Reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hartmann</LastName>
<ForeName>Boris M</ForeName>
<Initials>BM</Initials>
<AffiliationInfo><Affiliation>Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA Center for Translational Systems Biology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Thakar</LastName>
<ForeName>Juilee</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, Yale School of Medicine, New Haven, Connecticut, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Albrecht</LastName>
<ForeName>Randy A</ForeName>
<Initials>RA</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York, USA Global Health & Emerging Pathogens Institute at Icahn School of Medicine, New York, New York, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Avey</LastName>
<ForeName>Stefan</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Interdepartmental Program in Computational Biology and Bioinformatics, Yale University, New Haven, Connecticut, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zaslavsky</LastName>
<ForeName>Elena</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA Center for Translational Systems Biology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Marjanovic</LastName>
<ForeName>Nada</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chikina</LastName>
<ForeName>Maria</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fribourg</LastName>
<ForeName>Miguel</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hayot</LastName>
<ForeName>Fernand</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA Center for Translational Systems Biology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schmolke</LastName>
<ForeName>Mirco</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Molecular Medicine, University of Geneva, Geneva, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Meng</LastName>
<ForeName>Hailong</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, Yale School of Medicine, New Haven, Connecticut, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wetmur</LastName>
<ForeName>James</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>García-Sastre</LastName>
<ForeName>Adolfo</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York, USA Global Health & Emerging Pathogens Institute at Icahn School of Medicine, New York, New York, USA Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kleinstein</LastName>
<ForeName>Steven H</ForeName>
<Initials>SH</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, Yale School of Medicine, New Haven, Connecticut, USA Interdepartmental Program in Computational Biology and Bioinformatics, Yale University, New Haven, Connecticut, USA steven.kleinstein@yale.edu stuart.sealfon@mssm.edu.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sealfon</LastName>
<ForeName>Stuart C</ForeName>
<Initials>SC</Initials>
<AffiliationInfo><Affiliation>Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA Center for Translational Systems Biology, Icahn School of Medicine at Mount Sinai, New York, New York, USA steven.kleinstein@yale.edu stuart.sealfon@mssm.edu.</Affiliation>
</AffiliationInfo>
</Author>
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<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>HHSN272201000054C</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>U19 AI117873</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>HHSN272201000054C</GrantID>
<Agency>PHS HHS</Agency>
<Country>United States</Country>
</Grant>
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<PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2015</Year>
<Month>07</Month>
<Day>29</Day>
</ArticleDate>
</Article>
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<MedlineTA>J Virol</MedlineTA>
<NlmUniqueID>0113724</NlmUniqueID>
<ISSNLinking>0022-538X</ISSNLinking>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>9008-11-1</RegistryNumber>
<NameOfSubstance UI="D007372">Interferons</NameOfSubstance>
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<CitationSubset>IM</CitationSubset>
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Human Dendritic Cell Response Signatures Distinguish 1918, Pandemic, and Seasonal H1N1 Influenza Viruses.

Human Dendritic Cell Response Signatures Distinguish 1918, Pandemic, and Seasonal H1N1 Influenza Viruses.

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