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
Url:
DOI: 10.1042/BSR20181059
PubMed: 30242057
PubMed Central: 6200698
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<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>
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<title-group><article-title>Overexpression of the nucleocapsid protein of Middle East respiratory syndrome coronavirus up-regulates CXCL10</article-title>
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<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>
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<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>
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<xref ref-type="aff" rid="A2"><sup>2</sup>
</xref>
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<contrib contrib-type="author"><name><surname>Monteil</surname>
<given-names>Vanessa M.</given-names>
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<xref ref-type="aff" rid="A3"><sup>3</sup>
</xref>
<xref ref-type="aff" rid="A4"><sup>4</sup>
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<contrib contrib-type="author"><name><surname>Mirazimi</surname>
<given-names>Ali</given-names>
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<xref ref-type="aff" rid="A3"><sup>3</sup>
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<xref ref-type="aff" rid="A4"><sup>4</sup>
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<name><surname>Tan</surname>
<given-names>Yee-Joo</given-names>
</name>
<xref ref-type="aff" rid="A1"><sup>1</sup>
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<xref ref-type="aff" rid="A2"><sup>2</sup>
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</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>
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