Interferon priming enables cells to partially overturn the SARS coronavirus-induced block in innate immune activation.
Identifieur interne : 001851 ( PubMed/Checkpoint ); précédent : 001850; suivant : 001852Interferon priming enables cells to partially overturn the SARS coronavirus-induced block in innate immune activation.
Auteurs : Thomas Kuri [Allemagne] ; Xiaonan Zhang [République populaire de Chine] ; Matthias Habjan [Allemagne] ; Luis Martínez-Sobrido [États-Unis] ; Adolfo García-Sastre [États-Unis] ; Zhenghong Yuan [République populaire de Chine] ; Friedemann Weber [Allemagne]Source :
- The Journal of general virology [ 1465-2099 ] ; 2009.
Descripteurs français
- KwdFr :
- MESH :
- immunologie : Interféron alpha, Virus du SRAS.
- métabolisme : Cytokines, Facteur-3 de régulation d'interféron, Facteur-7 de régulation d'interféron.
- Animaux, Humains, Lignée cellulaire, Noyau de la cellule, Transport de protéines.
English descriptors
- KwdEn :
- MESH :
- chemical , immunology : Interferon-alpha.
- chemical , metabolism : Cytokines, Interferon Regulatory Factor-3, Interferon Regulatory Factor-7.
- chemistry : Cell Nucleus.
- immunology : SARS Virus.
- Animals, Cell Line, Chlorocebus aethiops, Humans, Protein Transport.
Abstract
SARS coronavirus (SARS-CoV) is known to efficiently suppress the induction of antiviral type I interferons (IFN-alpha/beta) in non-lymphatic cells through inhibition of the transcription factor IRF-3. Plasmacytoid dendritic cells, in contrast, respond to infection with production of high levels of IFNs. Here, we show that pretreatment of non-lymphatic cells with small amounts of IFN-alpha (IFN priming) partially overturns the block in IFN induction imposed by SARS-CoV. IFN priming combined with SARS-CoV infection substantially induced genes for IFN induction, IFN signalling, antiviral effector proteins, ubiquitination and ISGylation, antigen presentation and other cytokines and chemokines, whereas each individual treatment had no major effect. Curiously, however, despite this typical IFN response, neither IRF-3 nor IRF-7 was transported to the nucleus as a sign of activation. Taken together, our results suggest that (i) IFN, as it is produced by plasmacytoid dendritic cells, could enable tissue cells to launch a host response to SARS-CoV, (ii) IRF-3 and IRF-7 may be active at subdetectable levels, and (iii) SARS-CoV does not activate IRF-7.
DOI: 10.1099/vir.0.013599-0
PubMed: 19625461
Affiliations:
- Allemagne, République populaire de Chine, États-Unis
- Bade-Wurtemberg, District de Fribourg-en-Brisgau, État de New York
- Fribourg-en-Brisgau
Links toward previous steps (curation, corpus...)
Links to Exploration step
pubmed:19625461Le document en format XML
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uniqKey="Kuri T" first="Thomas" last="Kuri">Thomas Kuri</name><affiliation wicri:level="3"><nlm:affiliation>Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, D-79008 Freiburg, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, D-79008 Freiburg</wicri:regionArea><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Fribourg-en-Brisgau</region><settlement type="city">Fribourg-en-Brisgau</settlement></placeName></affiliation></author><author><name sortKey="Zhang, Xiaonan" sort="Zhang, Xiaonan" uniqKey="Zhang X" first="Xiaonan" last="Zhang">Xiaonan Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Research Unit, Shanghai Public Health Clinical Center, and Key Laboratory of Medical Molecular Virology, Fudan University, Shanghai, PR China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Research Unit, Shanghai Public Health Clinical Center, and Key Laboratory of Medical Molecular Virology, Fudan University, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Habjan, Matthias" sort="Habjan, Matthias" uniqKey="Habjan M" first="Matthias" last="Habjan">Matthias Habjan</name><affiliation wicri:level="3"><nlm:affiliation>Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, D-79008 Freiburg, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, D-79008 Freiburg</wicri:regionArea><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Fribourg-en-Brisgau</region><settlement type="city">Fribourg-en-Brisgau</settlement></placeName></affiliation></author><author><name sortKey="Martinez Sobrido, Luis" sort="Martinez Sobrido, Luis" uniqKey="Martinez Sobrido L" first="Luis" last="Martínez-Sobrido">Luis Martínez-Sobrido</name><affiliation wicri:level="2"><nlm:affiliation>School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Garcia Sastre, Adolfo" sort="Garcia Sastre, Adolfo" uniqKey="Garcia Sastre A" first="Adolfo" last="García-Sastre">Adolfo García-Sastre</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology, Department of Medicine (Division of Infectious Diseases) and Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine, New York, NY 10029, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology, Department of Medicine (Division of Infectious Diseases) and Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine, New York, NY 10029</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Yuan, Zhenghong" sort="Yuan, Zhenghong" uniqKey="Yuan Z" first="Zhenghong" last="Yuan">Zhenghong Yuan</name><affiliation wicri:level="1"><nlm:affiliation>Research Unit, Shanghai Public Health Clinical Center, and Key Laboratory of Medical Molecular Virology, Fudan University, Shanghai, PR China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Research Unit, Shanghai Public Health Clinical Center, and Key Laboratory of Medical Molecular Virology, Fudan University, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Weber, Friedemann" sort="Weber, Friedemann" uniqKey="Weber F" first="Friedemann" last="Weber">Friedemann Weber</name><affiliation wicri:level="3"><nlm:affiliation>Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, D-79008 Freiburg, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, D-79008 Freiburg</wicri:regionArea><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Fribourg-en-Brisgau</region><settlement type="city">Fribourg-en-Brisgau</settlement></placeName></affiliation></author></analytic><series><title level="j">The Journal of general virology</title><idno type="eISSN">1465-2099</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Cell Nucleus (chemistry)</term><term>Chlorocebus aethiops</term><term>Cytokines (metabolism)</term><term>Humans</term><term>Interferon Regulatory Factor-3 (metabolism)</term><term>Interferon Regulatory Factor-7 (metabolism)</term><term>Interferon-alpha (immunology)</term><term>Protein Transport</term><term>SARS Virus (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Cytokines (métabolisme)</term><term>Facteur-3 de régulation d'interféron (métabolisme)</term><term>Facteur-7 de régulation d'interféron (métabolisme)</term><term>Humains</term><term>Interféron alpha (immunologie)</term><term>Lignée cellulaire</term><term>Noyau de la cellule ()</term><term>Transport de protéines</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Interferon-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>Interferon Regulatory Factor-3</term><term>Interferon Regulatory Factor-7</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Cell Nucleus</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Interféron alpha</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term><term>Facteur-3 de régulation d'interféron</term><term>Facteur-7 de régulation d'interféron</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Chlorocebus aethiops</term><term>Humans</term><term>Protein Transport</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Lignée cellulaire</term><term>Noyau de la cellule</term><term>Transport de protéines</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">SARS coronavirus (SARS-CoV) is known to efficiently suppress the induction of antiviral type I interferons (IFN-alpha/beta) in non-lymphatic cells through inhibition of the transcription factor IRF-3. Plasmacytoid dendritic cells, in contrast, respond to infection with production of high levels of IFNs. Here, we show that pretreatment of non-lymphatic cells with small amounts of IFN-alpha (IFN priming) partially overturns the block in IFN induction imposed by SARS-CoV. IFN priming combined with SARS-CoV infection substantially induced genes for IFN induction, IFN signalling, antiviral effector proteins, ubiquitination and ISGylation, antigen presentation and other cytokines and chemokines, whereas each individual treatment had no major effect. Curiously, however, despite this typical IFN response, neither IRF-3 nor IRF-7 was transported to the nucleus as a sign of activation. Taken together, our results suggest that (i) IFN, as it is produced by plasmacytoid dendritic cells, could enable tissue cells to launch a host response to SARS-CoV, (ii) IRF-3 and IRF-7 may be active at subdetectable levels, and (iii) SARS-CoV does not activate IRF-7.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19625461</PMID><DateCompleted><Year>2009</Year><Month>10</Month><Day>30</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1465-2099</ISSN><JournalIssue CitedMedium="Internet"><Volume>90</Volume><Issue>Pt 11</Issue><PubDate><Year>2009</Year><Month>Nov</Month></PubDate></JournalIssue><Title>The Journal of general virology</Title><ISOAbbreviation>J. Gen. Virol.</ISOAbbreviation></Journal><ArticleTitle>Interferon priming enables cells to partially overturn the SARS coronavirus-induced block in innate immune activation.</ArticleTitle><Pagination><MedlinePgn>2686-2694</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1099/vir.0.013599-0</ELocationID><Abstract><AbstractText>SARS coronavirus (SARS-CoV) is known to efficiently suppress the induction of antiviral type I interferons (IFN-alpha/beta) in non-lymphatic cells through inhibition of the transcription factor IRF-3. Plasmacytoid dendritic cells, in contrast, respond to infection with production of high levels of IFNs. Here, we show that pretreatment of non-lymphatic cells with small amounts of IFN-alpha (IFN priming) partially overturns the block in IFN induction imposed by SARS-CoV. IFN priming combined with SARS-CoV infection substantially induced genes for IFN induction, IFN signalling, antiviral effector proteins, ubiquitination and ISGylation, antigen presentation and other cytokines and chemokines, whereas each individual treatment had no major effect. Curiously, however, despite this typical IFN response, neither IRF-3 nor IRF-7 was transported to the nucleus as a sign of activation. Taken together, our results suggest that (i) IFN, as it is produced by plasmacytoid dendritic cells, could enable tissue cells to launch a host response to SARS-CoV, (ii) IRF-3 and IRF-7 may be active at subdetectable levels, and (iii) SARS-CoV does not activate IRF-7.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kuri</LastName><ForeName>Thomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, D-79008 Freiburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Xiaonan</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Research Unit, Shanghai Public Health Clinical Center, and Key Laboratory of Medical Molecular Virology, Fudan University, Shanghai, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Habjan</LastName><ForeName>Matthias</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, D-79008 Freiburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martínez-Sobrido</LastName><ForeName>Luis</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>García-Sastre</LastName><ForeName>Adolfo</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Department of Medicine (Division of Infectious Diseases) and Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine, New York, NY 10029, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yuan</LastName><ForeName>Zhenghong</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Research Unit, Shanghai Public Health Clinical Center, and Key Laboratory of Medical Molecular Virology, Fudan University, Shanghai, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Weber</LastName><ForeName>Friedemann</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, D-79008 Freiburg, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>U19 AI062623</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U19AI62623</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal 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