MersV1, Main, Exploration, bibRecord, 000867

Overexpression of the nucleocapsid protein of Middle East respiratory syndrome coronavirus up-regulates CXCL10

Identifieur interne : 000867 ( Main/Exploration ); précédent : 000866; suivant : 000868

Overexpression 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.

RBID : PMC:6200698

Descripteurs français

English descriptors

KwdEn :
- A549 Cells, Chemokine CXCL10 (genetics), Coronavirus Infections (genetics), Coronavirus Infections (pathology), Coronavirus Infections (virology), Gene Expression Regulation, Viral (genetics), Host-Pathogen Interactions (genetics), Humans, Middle East Respiratory Syndrome Coronavirus (genetics), Middle East Respiratory Syndrome Coronavirus (pathogenicity), Nucleocapsid Proteins (genetics), Protein Domains (genetics), Transcriptional Activation (genetics).
MESH :
- chemical , genetics : Chemokine CXCL10, Nucleocapsid Proteins.
- genetics : Coronavirus Infections, Gene Expression Regulation, Viral, Host-Pathogen Interactions, Middle East Respiratory Syndrome Coronavirus, Protein Domains, Transcriptional Activation.
- pathogenicity : Middle East Respiratory Syndrome Coronavirus.
- pathology : Coronavirus Infections.
- virology : Coronavirus Infections.
- A549 Cells, Humans.

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 TNF, IL6, IL8, and CXCL10, 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.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6200698

DOI: 10.1042/BSR20181059
PubMed: 30242057
PubMed Central: 6200698

Affiliations:

Le document en format XML

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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>
</div>
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<author><name sortKey="Fehr, A R" uniqKey="Fehr A">A.R. Fehr</name>
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<author><name sortKey="Athmer, J" uniqKey="Athmer J">J. Athmer</name>
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</analytic>
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</author>
<author><name sortKey="Wang, H" uniqKey="Wang H">H. Wang</name>
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<author><name sortKey="Ji, Y" uniqKey="Ji Y">Y. Ji</name>
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</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Hsin, W C" uniqKey="Hsin W">W.C. Hsin</name>
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<author><name sortKey="Chang, C H" uniqKey="Chang C">C.H. Chang</name>
</author>
<author><name sortKey="Chang, C Y" uniqKey="Chang C">C.Y. Chang</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Mo, Y" uniqKey="Mo Y">Y. Mo</name>
</author>
<author><name sortKey="Fisher, D" uniqKey="Fisher D">D. Fisher</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Lau, S K" uniqKey="Lau S">S.K. Lau</name>
</author>
<author><name sortKey="Lau, C C" uniqKey="Lau C">C.C. Lau</name>
</author>
<author><name sortKey="Chan, K H" uniqKey="Chan K">K.H. Chan</name>
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</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Faure, E" uniqKey="Faure E">E. Faure</name>
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<author><name sortKey="Poissy, J" uniqKey="Poissy J">J. Poissy</name>
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<author><name sortKey="Goffard, A" uniqKey="Goffard A">A. Goffard</name>
</author>
</analytic>
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</author>
<author><name sortKey="Park, W B" uniqKey="Park W">W.B. Park</name>
</author>
</analytic>
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</author>
<author><name sortKey="Zhou, J" uniqKey="Zhou J">J. Zhou</name>
</author>
<author><name sortKey="Wong, B H" uniqKey="Wong B">B.H. Wong</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Oh, H L" uniqKey="Oh H">H.L. Oh</name>
</author>
<author><name sortKey="Akerstrom, S" uniqKey="Akerstrom S">S. Akerstrom</name>
</author>
<author><name sortKey="Shen, S" uniqKey="Shen S">S. Shen</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Chan, J F" uniqKey="Chan J">J.F. Chan</name>
</author>
<author><name sortKey="Chan, K H" uniqKey="Chan K">K.H. Chan</name>
</author>
<author><name sortKey="Choi, G K" uniqKey="Choi G">G.K. Choi</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Tynell, J" uniqKey="Tynell J">J. Tynell</name>
</author>
<author><name sortKey="Westenius, V" uniqKey="Westenius V">V. Westenius</name>
</author>
<author><name sortKey="Ronkko, E" uniqKey="Ronkko E">E. Ronkko</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Liu, M" uniqKey="Liu M">M. Liu</name>
</author>
<author><name sortKey="Guo, S" uniqKey="Guo S">S. Guo</name>
</author>
<author><name sortKey="Hibbert, J M" uniqKey="Hibbert J">J.M. Hibbert</name>
</author>
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</TEI>
<affiliations><list><country><li>Singapour</li>
<li>Suède</li>
</country>
<region><li>Svealand</li>
</region>
<settlement><li>Stockholm</li>
</settlement>
<orgName><li>Université nationale de Singapour</li>
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</list>
<tree><country name="Singapour"><noRegion><name sortKey="Aboagye, James Odame" sort="Aboagye, James Odame" uniqKey="Aboagye J" first="James Odame" last="Aboagye">James Odame Aboagye</name>
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<name sortKey="Aboagye, James Odame" sort="Aboagye, James Odame" uniqKey="Aboagye J" first="James Odame" last="Aboagye">James Odame Aboagye</name>
<name sortKey="Ng, Oi Wing" sort="Ng, Oi Wing" uniqKey="Ng O" first="Oi-Wing" last="Ng">Oi-Wing Ng</name>
<name sortKey="Tan, Yee Joo" sort="Tan, Yee Joo" uniqKey="Tan Y" first="Yee-Joo" last="Tan">Yee-Joo Tan</name>
<name sortKey="Tan, Yee Joo" sort="Tan, Yee Joo" uniqKey="Tan Y" first="Yee-Joo" last="Tan">Yee-Joo Tan</name>
<name sortKey="Yew, Chow Wenn" sort="Yew, Chow Wenn" uniqKey="Yew C" first="Chow Wenn" last="Yew">Chow Wenn Yew</name>
</country>
<country name="Suède"><noRegion><name sortKey="Monteil, Vanessa M" sort="Monteil, Vanessa M" uniqKey="Monteil V" first="Vanessa M." last="Monteil">Vanessa M. Monteil</name>
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<name sortKey="Mirazimi, Ali" sort="Mirazimi, Ali" uniqKey="Mirazimi A" first="Ali" last="Mirazimi">Ali Mirazimi</name>
<name sortKey="Mirazimi, Ali" sort="Mirazimi, Ali" uniqKey="Mirazimi A" first="Ali" last="Mirazimi">Ali Mirazimi</name>
<name sortKey="Monteil, Vanessa M" sort="Monteil, Vanessa M" uniqKey="Monteil V" first="Vanessa M." last="Monteil">Vanessa M. Monteil</name>
</country>
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</affiliations>
</record>

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   |texte=   Overexpression of the nucleocapsid protein of Middle East respiratory syndrome coronavirus up-regulates CXCL10
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Serveur d'exploration MERS

Overexpression of the nucleocapsid protein of Middle East respiratory syndrome coronavirus up-regulates CXCL10

Overexpression of the nucleocapsid protein of Middle East respiratory syndrome coronavirus up-regulates CXCL10

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	Serveur d'exploration MERS
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