Overexpression of the nucleocapsid protein of Middle East respiratory syndrome coronavirus up-regulates CXCL10
Identifieur interne : 000B40 ( Pmc/Curation ); précédent : 000B39; suivant : 000B41Overexpression of the nucleocapsid protein of Middle East respiratory syndrome coronavirus up-regulates CXCL10
Auteurs : James Odame Aboagye [Singapour] ; Chow Wenn Yew [Singapour] ; Oi-Wing Ng [Singapour] ; Vanessa M. Monteil [Suède] ; Ali Mirazimi [Suède] ; Yee-Joo Tan [Singapour]Source :
- Bioscience Reports [ 0144-8463 ] ; 2018.
Abstract
Middle East respiratory syndrome coronavirus (MERS-CoV) causes respiratory diseases in humans and has a high mortality rate. During infection, MERS-CoV regulates several host cellular processes including antiviral response genes. In order to determine if the nucleocapsid protein of MERS-CoV (MERS-N) plays a role in viral–host interactions, a murine monoclonal antibody was generated so as to allow detection of the protein in infected cells as well as in overexpression system. Then, MERS-N was stably overexpressed in A549 cells, and a PCR array containing 84 genes was used to screen for genes transcriptionally regulated by it. Several up-regulated antiviral genes, namely
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DOI: 10.1042/BSR20181059
PubMed: 30242057
PubMed Central: 6200698
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Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University Health System (NUHS), National University of Singapore</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">30242057</idno><idno type="pmc">6200698</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6200698</idno><idno type="RBID">PMC:6200698</idno><idno type="doi">10.1042/BSR20181059</idno><date when="2018">2018</date><idno type="wicri:Area/Pmc/Corpus">000B40</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000B40</idno><idno type="wicri:Area/Pmc/Curation">000B40</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000B40</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Overexpression of the nucleocapsid protein of Middle East respiratory syndrome coronavirus up-regulates CXCL10</title><author><name sortKey="Aboagye, James Odame" sort="Aboagye, James Odame" uniqKey="Aboagye J" first="James Odame" last="Aboagye">James Odame Aboagye</name><affiliation wicri:level="1"><nlm:aff id="A1">Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR)</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="A2">Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University Health System (NUHS), National University of Singapore, Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University Health System (NUHS), National University of Singapore</wicri:regionArea></affiliation></author><author><name sortKey="Yew, Chow Wenn" sort="Yew, Chow Wenn" uniqKey="Yew C" first="Chow Wenn" last="Yew">Chow Wenn Yew</name><affiliation wicri:level="1"><nlm:aff id="A1">Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR)</wicri:regionArea></affiliation></author><author><name sortKey="Ng, Oi Wing" sort="Ng, Oi Wing" uniqKey="Ng O" first="Oi-Wing" last="Ng">Oi-Wing Ng</name><affiliation wicri:level="1"><nlm:aff id="A2">Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University Health System (NUHS), National University of Singapore, Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University Health System (NUHS), National University of Singapore</wicri:regionArea></affiliation></author><author><name sortKey="Monteil, Vanessa M" sort="Monteil, Vanessa M" uniqKey="Monteil V" first="Vanessa M." last="Monteil">Vanessa M. Monteil</name><affiliation wicri:level="1"><nlm:aff id="A3">Department for Laboratory Medicine, Karolinska Institute and Karolinska Hospital University, Solna, Sweden</nlm:aff><country xml:lang="fr">Suède</country><wicri:regionArea>Department for Laboratory Medicine, Karolinska Institute and Karolinska Hospital University, Solna</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="A4">Public Health Agency of Sweden, Stockholm, Sweden</nlm:aff><country xml:lang="fr">Suède</country><wicri:regionArea>Public Health Agency of Sweden, Stockholm</wicri:regionArea></affiliation></author><author><name sortKey="Mirazimi, Ali" sort="Mirazimi, Ali" uniqKey="Mirazimi A" first="Ali" last="Mirazimi">Ali Mirazimi</name><affiliation wicri:level="1"><nlm:aff id="A3">Department for Laboratory Medicine, Karolinska Institute and Karolinska Hospital University, Solna, Sweden</nlm:aff><country xml:lang="fr">Suède</country><wicri:regionArea>Department for Laboratory Medicine, Karolinska Institute and Karolinska Hospital University, Solna</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="A4">Public Health Agency of Sweden, Stockholm, Sweden</nlm:aff><country xml:lang="fr">Suède</country><wicri:regionArea>Public Health Agency of Sweden, Stockholm</wicri:regionArea></affiliation></author><author><name sortKey="Tan, Yee Joo" sort="Tan, Yee Joo" uniqKey="Tan Y" first="Yee-Joo" last="Tan">Yee-Joo Tan</name><affiliation wicri:level="1"><nlm:aff id="A1">Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR)</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="A2">Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University Health System (NUHS), National University of Singapore, Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University Health System (NUHS), National University of Singapore</wicri:regionArea></affiliation></author></analytic><series><title level="j">Bioscience Reports</title><idno type="ISSN">0144-8463</idno><idno type="eISSN">1573-4935</idno><imprint><date when="2018">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Middle East respiratory syndrome coronavirus (MERS-CoV) causes respiratory diseases in humans and has a high mortality rate. During infection, MERS-CoV regulates several host cellular processes including antiviral response genes. In order to determine if the nucleocapsid protein of MERS-CoV (MERS-N) plays a role in viral–host interactions, a murine monoclonal antibody was generated so as to allow detection of the protein in infected cells as well as in overexpression system. Then, MERS-N was stably overexpressed in A549 cells, and a PCR array containing 84 genes was used to screen for genes transcriptionally regulated by it. Several up-regulated antiviral genes, namely <italic>TNF, IL6, IL8</italic>, and <italic>CXCL10</italic>, were selected for independent validation in transiently transfected 293FT cells. Out of these, the overexpression of MERS-N was found to up-regulate CXCL10 at both transcriptional and translational levels. Interestingly, CXCL10 has been reported to be up-regulated in MERS-CoV infected airway epithelial cells and lung fibroblast cells, as well as monocyte-derived macrophages and dendritic cells. High secretions and persistent increase of CXCL10 in MERS-CoV patients have been also associated with severity of disease. To our knowledge, this is the first report showing that the MERS-N protein is one of the contributing factors for CXCL10 up-regulation during infection. In addition, our results showed that a fragment consisting of residues 196–413 in MERS-N is sufficient to up-regulate CXCL10, while the N-terminal domain and serine-arginine (SR)-rich motif of MERS-N do not play a role in this up-regulation.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Channappanavar, R" uniqKey="Channappanavar R">R. Channappanavar</name></author><author><name sortKey="Perlman, S" uniqKey="Perlman S">S. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Biosci Rep</journal-id><journal-id journal-id-type="iso-abbrev">Biosci. Rep</journal-id><journal-id journal-id-type="hwp">ppbioscirep</journal-id><journal-id journal-id-type="publisher-id">BSR</journal-id><journal-title-group><journal-title>Bioscience Reports</journal-title></journal-title-group><issn pub-type="ppub">0144-8463</issn><issn pub-type="epub">1573-4935</issn><publisher><publisher-name>Portland Press Ltd.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">30242057</article-id><article-id pub-id-type="pmc">6200698</article-id><article-id pub-id-type="doi">10.1042/BSR20181059</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Articles</subject></subj-group><subj-group subj-group-type="overline"><subject>Research Article</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>33</subject><subject>37</subject><subject>45</subject></subj-group></article-categories><title-group><article-title>Overexpression of the nucleocapsid protein of Middle East respiratory syndrome coronavirus up-regulates CXCL10</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Aboagye</surname><given-names>James Odame</given-names></name><xref ref-type="aff" rid="A1"><sup>1</sup></xref><xref ref-type="aff" rid="A2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Yew</surname><given-names>Chow Wenn</given-names></name><xref ref-type="aff" rid="A1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Ng</surname><given-names>Oi-Wing</given-names></name><xref ref-type="aff" rid="A2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Monteil</surname><given-names>Vanessa M.</given-names></name><xref ref-type="aff" rid="A3"><sup>3</sup></xref><xref ref-type="aff" rid="A4"><sup>4</sup></xref></contrib><contrib contrib-type="author"><name><surname>Mirazimi</surname><given-names>Ali</given-names></name><xref ref-type="aff" rid="A3"><sup>3</sup></xref><xref ref-type="aff" rid="A4"><sup>4</sup></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0002-2278-4497</contrib-id><name><surname>Tan</surname><given-names>Yee-Joo</given-names></name><xref ref-type="aff" rid="A1"><sup>1</sup></xref><xref ref-type="aff" rid="A2"><sup>2</sup></xref><xref ref-type="corresp" rid="COR1"></xref></contrib><aff id="A1"><label>1</label>Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore</aff><aff id="A2"><label>2</label>Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University Health System (NUHS), National University of Singapore, Singapore</aff><aff id="A3"><label>3</label>Department for Laboratory Medicine, Karolinska Institute and Karolinska Hospital University, Solna, Sweden</aff><aff id="A4"><label>4</label>Public Health Agency of Sweden, Stockholm, Sweden</aff></contrib-group><author-notes><corresp id="COR1"><bold>Correspondence:</bold> Yee-Joo Tan (<email>yee_joo_tan@nuhs.edu.sg</email>)</corresp></author-notes><pub-date pub-type="epreprint"><day>21</day><month>9</month><year>2018</year></pub-date><pub-date pub-type="collection"><day>31</day><month>10</month><year>2018</year></pub-date><pub-date pub-type="epub"><day>17</day><month>10</month><year>2018</year></pub-date><volume>38</volume><issue>5</issue><elocation-id>BSR20181059</elocation-id><history><date date-type="received"><day>01</day><month>7</month><year>2018</year></date><date date-type="rev-recd"><day>16</day><month>9</month><year>2018</year></date><date date-type="accepted"><day>18</day><month>9</month><year>2018</year></date></history><permissions><copyright-statement>© 2018 The Author(s).</copyright-statement><copyright-year>2018</copyright-year><license license-type="open-access"><ali:license_ref>http://creativecommons.org/licenses/by/4.0/</ali:license_ref><license-p>This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">Creative Commons Attribution License 4.0 (CC BY)</ext-link>.</license-p></license></permissions><self-uri xlink:title="pdf" xlink:href="bsr-38-bsr20181059.pdf"></self-uri><abstract><p>Middle East respiratory syndrome coronavirus (MERS-CoV) causes respiratory diseases in humans and has a high mortality rate. During infection, MERS-CoV regulates several host cellular processes including antiviral response genes. In order to determine if the nucleocapsid protein of MERS-CoV (MERS-N) plays a role in viral–host interactions, a murine monoclonal antibody was generated so as to allow detection of the protein in infected cells as well as in overexpression system. Then, MERS-N was stably overexpressed in A549 cells, and a PCR array containing 84 genes was used to screen for genes transcriptionally regulated by it. Several up-regulated antiviral genes, namely <italic>TNF, IL6, IL8</italic>, and <italic>CXCL10</italic>, were selected for independent validation in transiently transfected 293FT cells. Out of these, the overexpression of MERS-N was found to up-regulate CXCL10 at both transcriptional and translational levels. Interestingly, CXCL10 has been reported to be up-regulated in MERS-CoV infected airway epithelial cells and lung fibroblast cells, as well as monocyte-derived macrophages and dendritic cells. High secretions and persistent increase of CXCL10 in MERS-CoV patients have been also associated with severity of disease. To our knowledge, this is the first report showing that the MERS-N protein is one of the contributing factors for CXCL10 up-regulation during infection. In addition, our results showed that a fragment consisting of residues 196–413 in MERS-N is sufficient to up-regulate CXCL10, while the N-terminal domain and serine-arginine (SR)-rich motif of MERS-N do not play a role in this up-regulation.</p></abstract><kwd-group><kwd>CXCL10</kwd><kwd>Middle East Respiratory Syndrome coronavirus</kwd><kwd>nucleocapsid</kwd></kwd-group><counts><page-count count="10"></page-count></counts></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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|area= MersV1
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|texte= Overexpression of the nucleocapsid protein of Middle East respiratory syndrome coronavirus up-regulates CXCL10
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