Delayed induction of proinflammatory cytokines and suppression of innate antiviral response by the novel Middle East respiratory syndrome coronavirus: implications for pathogenesis and treatment.
Identifieur interne : 001B71 ( PubMed/Corpus ); précédent : 001B70; suivant : 001B72Delayed induction of proinflammatory cytokines and suppression of innate antiviral response by the novel Middle East respiratory syndrome coronavirus: implications for pathogenesis and treatment.
Auteurs : Susanna K P. Lau ; Candy C Y. Lau ; Kwok-Hung Chan ; Clara P Y. Li ; Honglin Chen ; Dong-Yan Jin ; Jasper F W. Chan ; Patrick C Y. Woo ; Kwok-Yung YuenSource :
- The Journal of general virology [ 1465-2099 ] ; 2013.
English descriptors
- KwdEn :
- Bronchi (cytology), Bronchi (virology), Cell Line, Coronavirus (immunology), Coronavirus (pathogenicity), Coronavirus (physiology), Cytokines (genetics), Cytokines (metabolism), Epithelial Cells (immunology), Epithelial Cells (virology), Fibroblasts (virology), Gene Expression Regulation (immunology), Humans, Immunity, Innate, Inflammation (immunology), Inflammation (metabolism), Middle East, Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (therapy), Viral Load, Virus Replication.
- MESH :
- chemical , genetics : Cytokines.
- geographic : Middle East.
- cytology : Bronchi.
- immunology : Coronavirus, Epithelial Cells, Gene Expression Regulation, Inflammation, Severe Acute Respiratory Syndrome.
- chemical , metabolism : Cytokines, Inflammation.
- pathogenicity : Coronavirus.
- physiology : Coronavirus.
- therapy : Severe Acute Respiratory Syndrome.
- virology : Bronchi, Epithelial Cells, Fibroblasts.
- Cell Line, Humans, Immunity, Innate, Viral Load, Virus Replication.
Abstract
The high mortality associated with the novel Middle East respiratory syndrome coronavirus (MERS-CoV) has raised questions about the possible role of a cytokine storm in its pathogenesis. Although recent studies showed that MERS-CoV infection is associated with an attenuated IFN response, no induction of inflammatory cytokines was demonstrated during the early phase of infection. To study both early and late cytokine responses associated with MERS-CoV infection, we measured the mRNA levels of eight cytokine genes [TNF-α, IL-1β, IL-6, IL-8, IFN-β, monocyte chemotactic protein-1, transforming growth factor-β and IFN-γ-induced protein (IP)-10] in cell lysates of polarized airway epithelial Calu-3 cells infected with MERS-CoV or severe acute respiratory syndrome (SARS)-CoV up to 30 h post-infection. Among the eight cytokine genes, IL-1β, IL-6 and IL-8 induced by MERS-CoV were markedly higher than those induced by SARS-CoV at 30 h, whilst TNF-α, IFN-β and IP-10 induced by SARS-CoV were markedly higher than those induced by MERS-CoV at 24 and 30 h in infected Calu-3 cells. The activation of IL-8 and attenuated IFN-β response by MERS-CoV were also confirmed by protein measurements in the culture supernatant when compared with SARS-CoV and Sendai virus. To further confirm the attenuated antiviral response, cytokine response was compared with human HCoV-229E in embryonal lung fibroblast HFL cells, which also revealed higher IFN-β and IP-10 levels induced by HCoV-229E than MERS-CoV at 24 and 30 h. Whilst our data supported recent findings that MERS-CoV elicits attenuated innate immunity, this represents the first report to demonstrate delayed proinflammatory cytokine induction by MERS-CoV. Our results provide insights into the pathogenesis and treatment of MERS-CoV infections.
DOI: 10.1099/vir.0.055533-0
PubMed: 24077366
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pubmed:24077366Le document en format XML
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China.</nlm:affiliation></affiliation></author><author><name sortKey="Chan, Kwok Hung" sort="Chan, Kwok Hung" uniqKey="Chan K" first="Kwok-Hung" last="Chan">Kwok-Hung Chan</name><affiliation><nlm:affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Clara P Y" sort="Li, Clara P Y" uniqKey="Li C" first="Clara P Y" last="Li">Clara P Y. Li</name><affiliation><nlm:affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Honglin" sort="Chen, Honglin" uniqKey="Chen H" first="Honglin" last="Chen">Honglin Chen</name><affiliation><nlm:affiliation>Research Centre of Infection and Immunology, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Jin, Dong Yan" sort="Jin, Dong Yan" uniqKey="Jin D" first="Dong-Yan" last="Jin">Dong-Yan Jin</name><affiliation><nlm:affiliation>Department of Biochemistry, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Chan, Jasper F W" sort="Chan, Jasper F W" uniqKey="Chan J" first="Jasper F W" last="Chan">Jasper F W. Chan</name><affiliation><nlm:affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Woo, Patrick C Y" sort="Woo, Patrick C Y" uniqKey="Woo P" first="Patrick C Y" last="Woo">Patrick C Y. Woo</name><affiliation><nlm:affiliation>Carol Yu Centre for Infection, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Yuen, Kwok Yung" sort="Yuen, Kwok Yung" uniqKey="Yuen K" first="Kwok-Yung" last="Yuen">Kwok-Yung Yuen</name><affiliation><nlm:affiliation>State Key Laboratory of Emerging Infectious Diseases, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:24077366</idno><idno type="pmid">24077366</idno><idno type="doi">10.1099/vir.0.055533-0</idno><idno type="wicri:Area/PubMed/Corpus">001B71</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001B71</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Delayed induction of proinflammatory cytokines and suppression of innate antiviral response by the novel Middle East respiratory syndrome coronavirus: implications for pathogenesis and treatment.</title><author><name sortKey="Lau, Susanna K P" sort="Lau, Susanna K P" uniqKey="Lau S" first="Susanna K P" last="Lau">Susanna K P. Lau</name><affiliation><nlm:affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Lau, Candy C Y" sort="Lau, Candy C Y" uniqKey="Lau C" first="Candy C Y" last="Lau">Candy C Y. Lau</name><affiliation><nlm:affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Chan, Kwok Hung" sort="Chan, Kwok Hung" uniqKey="Chan K" first="Kwok-Hung" last="Chan">Kwok-Hung Chan</name><affiliation><nlm:affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Clara P Y" sort="Li, Clara P Y" uniqKey="Li C" first="Clara P Y" last="Li">Clara P Y. Li</name><affiliation><nlm:affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Honglin" sort="Chen, Honglin" uniqKey="Chen H" first="Honglin" last="Chen">Honglin Chen</name><affiliation><nlm:affiliation>Research Centre of Infection and Immunology, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Jin, Dong Yan" sort="Jin, Dong Yan" uniqKey="Jin D" first="Dong-Yan" last="Jin">Dong-Yan Jin</name><affiliation><nlm:affiliation>Department of Biochemistry, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Chan, Jasper F W" sort="Chan, Jasper F W" uniqKey="Chan J" first="Jasper F W" last="Chan">Jasper F W. Chan</name><affiliation><nlm:affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Woo, Patrick C Y" sort="Woo, Patrick C Y" uniqKey="Woo P" first="Patrick C Y" last="Woo">Patrick C Y. Woo</name><affiliation><nlm:affiliation>Carol Yu Centre for Infection, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Yuen, Kwok Yung" sort="Yuen, Kwok Yung" uniqKey="Yuen K" first="Kwok-Yung" last="Yuen">Kwok-Yung Yuen</name><affiliation><nlm:affiliation>State Key Laboratory of Emerging Infectious Diseases, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation></affiliation></author></analytic><series><title level="j">The Journal of general virology</title><idno type="eISSN">1465-2099</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Bronchi (cytology)</term><term>Bronchi (virology)</term><term>Cell Line</term><term>Coronavirus (immunology)</term><term>Coronavirus (pathogenicity)</term><term>Coronavirus (physiology)</term><term>Cytokines (genetics)</term><term>Cytokines (metabolism)</term><term>Epithelial Cells (immunology)</term><term>Epithelial Cells (virology)</term><term>Fibroblasts (virology)</term><term>Gene Expression Regulation (immunology)</term><term>Humans</term><term>Immunity, Innate</term><term>Inflammation (immunology)</term><term>Inflammation (metabolism)</term><term>Middle East</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (therapy)</term><term>Viral Load</term><term>Virus Replication</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" type="geographic" xml:lang="en"><term>Middle East</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Bronchi</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Coronavirus</term><term>Epithelial Cells</term><term>Gene Expression Regulation</term><term>Inflammation</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Bronchi</term><term>Epithelial Cells</term><term>Fibroblasts</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Humans</term><term>Immunity, Innate</term><term>Viral Load</term><term>Virus Replication</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The high mortality associated with the novel Middle East respiratory syndrome coronavirus (MERS-CoV) has raised questions about the possible role of a cytokine storm in its pathogenesis. Although recent studies showed that MERS-CoV infection is associated with an attenuated IFN response, no induction of inflammatory cytokines was demonstrated during the early phase of infection. To study both early and late cytokine responses associated with MERS-CoV infection, we measured the mRNA levels of eight cytokine genes [TNF-α, IL-1β, IL-6, IL-8, IFN-β, monocyte chemotactic protein-1, transforming growth factor-β and IFN-γ-induced protein (IP)-10] in cell lysates of polarized airway epithelial Calu-3 cells infected with MERS-CoV or severe acute respiratory syndrome (SARS)-CoV up to 30 h post-infection. Among the eight cytokine genes, IL-1β, IL-6 and IL-8 induced by MERS-CoV were markedly higher than those induced by SARS-CoV at 30 h, whilst TNF-α, IFN-β and IP-10 induced by SARS-CoV were markedly higher than those induced by MERS-CoV at 24 and 30 h in infected Calu-3 cells. The activation of IL-8 and attenuated IFN-β response by MERS-CoV were also confirmed by protein measurements in the culture supernatant when compared with SARS-CoV and Sendai virus. To further confirm the attenuated antiviral response, cytokine response was compared with human HCoV-229E in embryonal lung fibroblast HFL cells, which also revealed higher IFN-β and IP-10 levels induced by HCoV-229E than MERS-CoV at 24 and 30 h. Whilst our data supported recent findings that MERS-CoV elicits attenuated innate immunity, this represents the first report to demonstrate delayed proinflammatory cytokine induction by MERS-CoV. Our results provide insights into the pathogenesis and treatment of MERS-CoV infections. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24077366</PMID><DateCompleted><Year>2014</Year><Month>01</Month><Day>21</Day></DateCompleted><DateRevised><Year>2020</Year><Month>02</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1465-2099</ISSN><JournalIssue CitedMedium="Internet"><Volume>94</Volume><Issue>Pt 12</Issue><PubDate><Year>2013</Year><Month>Dec</Month></PubDate></JournalIssue><Title>The Journal of general virology</Title><ISOAbbreviation>J. Gen. Virol.</ISOAbbreviation></Journal><ArticleTitle>Delayed induction of proinflammatory cytokines and suppression of innate antiviral response by the novel Middle East respiratory syndrome coronavirus: implications for pathogenesis and treatment.</ArticleTitle><Pagination><MedlinePgn>2679-2690</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1099/vir.0.055533-0</ELocationID><Abstract><AbstractText>The high mortality associated with the novel Middle East respiratory syndrome coronavirus (MERS-CoV) has raised questions about the possible role of a cytokine storm in its pathogenesis. Although recent studies showed that MERS-CoV infection is associated with an attenuated IFN response, no induction of inflammatory cytokines was demonstrated during the early phase of infection. To study both early and late cytokine responses associated with MERS-CoV infection, we measured the mRNA levels of eight cytokine genes [TNF-α, IL-1β, IL-6, IL-8, IFN-β, monocyte chemotactic protein-1, transforming growth factor-β and IFN-γ-induced protein (IP)-10] in cell lysates of polarized airway epithelial Calu-3 cells infected with MERS-CoV or severe acute respiratory syndrome (SARS)-CoV up to 30 h post-infection. Among the eight cytokine genes, IL-1β, IL-6 and IL-8 induced by MERS-CoV were markedly higher than those induced by SARS-CoV at 30 h, whilst TNF-α, IFN-β and IP-10 induced by SARS-CoV were markedly higher than those induced by MERS-CoV at 24 and 30 h in infected Calu-3 cells. The activation of IL-8 and attenuated IFN-β response by MERS-CoV were also confirmed by protein measurements in the culture supernatant when compared with SARS-CoV and Sendai virus. To further confirm the attenuated antiviral response, cytokine response was compared with human HCoV-229E in embryonal lung fibroblast HFL cells, which also revealed higher IFN-β and IP-10 levels induced by HCoV-229E than MERS-CoV at 24 and 30 h. Whilst our data supported recent findings that MERS-CoV elicits attenuated innate immunity, this represents the first report to demonstrate delayed proinflammatory cytokine induction by MERS-CoV. Our results provide insights into the pathogenesis and treatment of MERS-CoV infections. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lau</LastName><ForeName>Susanna K P</ForeName><Initials>SKP</Initials><AffiliationInfo><Affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>State Key Laboratory of Emerging Infectious Diseases, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Carol Yu Centre for Infection, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Centre of Infection and Immunology, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lau</LastName><ForeName>Candy C Y</ForeName><Initials>CCY</Initials><AffiliationInfo><Affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chan</LastName><ForeName>Kwok-Hung</ForeName><Initials>KH</Initials><AffiliationInfo><Affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Clara P Y</ForeName><Initials>CPY</Initials><AffiliationInfo><Affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Honglin</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Research Centre of Infection and Immunology, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Carol Yu Centre for Infection, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>State Key Laboratory of Emerging Infectious Diseases, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jin</LastName><ForeName>Dong-Yan</ForeName><Initials>DY</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chan</LastName><ForeName>Jasper F W</ForeName><Initials>JFW</Initials><AffiliationInfo><Affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Woo</LastName><ForeName>Patrick C Y</ForeName><Initials>PCY</Initials><AffiliationInfo><Affiliation>Carol Yu Centre for Infection, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>State Key Laboratory of Emerging Infectious Diseases, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Centre of Infection and Immunology, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yuen</LastName><ForeName>Kwok-Yung</ForeName><Initials>KY</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Emerging Infectious Diseases, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Centre of Infection and Immunology, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Carol Yu Centre for Infection, University of Hong Kong, Hong Kong, P.R. China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>09</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Gen Virol</MedlineTA><NlmUniqueID>0077340</NlmUniqueID><ISSNLinking>0022-1317</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001980" MajorTopicYN="N">Bronchi</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017934" MajorTopicYN="N">Coronavirus</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005347" MajorTopicYN="N">Fibroblasts</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007113" MajorTopicYN="N">Immunity, Innate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008877" MajorTopicYN="N" Type="Geographic">Middle East</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019562" MajorTopicYN="N">Viral Load</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>10</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>10</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>1</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24077366</ArticleId><ArticleId IdType="doi">10.1099/vir.0.055533-0</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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