Cell host response to infection with novel human coronavirus EMC predicts potential antivirals and important differences with SARS coronavirus.
Identifieur interne : 001214 ( PubMed/Checkpoint ); précédent : 001213; suivant : 001215Cell host response to infection with novel human coronavirus EMC predicts potential antivirals and important differences with SARS coronavirus.
Auteurs : Laurence Josset [États-Unis] ; Vineet D. Menachery ; Lisa E. Gralinski ; Sudhakar Agnihothram ; Pavel Sova ; Victoria S. Carter ; Boyd L. Yount ; Rachel L. Graham ; Ralph S. Baric ; Michael G. KatzeSource :
- mBio [ 2150-7511 ] ; 2013.
Descripteurs français
- KwdFr :
- Cellules épithéliales (immunologie), Cellules épithéliales (virologie), Coronavirus (isolement et purification), Coronavirus (pathogénicité), Coronavirus (physiologie), Humains, Interactions hôte-pathogène, Lignée cellulaire, Réplication virale, Syndrome respiratoire aigu sévère (virologie), Tolérance immunitaire, Transcriptome.
- MESH :
- immunologie : Cellules épithéliales.
- isolement et purification : Coronavirus.
- pathogénicité : Coronavirus.
- physiologie : Coronavirus.
- virologie : Cellules épithéliales, Syndrome respiratoire aigu sévère.
- Humains, Interactions hôte-pathogène, Lignée cellulaire, Réplication virale, Tolérance immunitaire, Transcriptome.
English descriptors
- KwdEn :
- MESH :
- immunology : Epithelial Cells.
- isolation & purification : Coronavirus.
- pathogenicity : Coronavirus.
- physiology : Coronavirus.
- virology : Epithelial Cells, Severe Acute Respiratory Syndrome.
- Cell Line, Host-Pathogen Interactions, Humans, Immune Tolerance, Transcriptome, Virus Replication.
Abstract
A novel human coronavirus (HCoV-EMC) was recently identified in the Middle East as the causative agent of a severe acute respiratory syndrome (SARS) resembling the illness caused by SARS coronavirus (SARS-CoV). Although derived from the CoV family, the two viruses are genetically distinct and do not use the same receptor. Here, we investigated whether HCoV-EMC and SARS-CoV induce similar or distinct host responses after infection of a human lung epithelial cell line. HCoV-EMC was able to replicate as efficiently as SARS-CoV in Calu-3 cells and similarly induced minimal transcriptomic changes before 12 h postinfection. Later in infection, HCoV-EMC induced a massive dysregulation of the host transcriptome, to a much greater extent than SARS-CoV. Both viruses induced a similar activation of pattern recognition receptors and the interleukin 17 (IL-17) pathway, but HCoV-EMC specifically down-regulated the expression of several genes within the antigen presentation pathway, including both type I and II major histocompatibility complex (MHC) genes. This could have an important impact on the ability of the host to mount an adaptive host response. A unique set of 207 genes was dysregulated early and permanently throughout infection with HCoV-EMC, and was used in a computational screen to predict potential antiviral compounds, including kinase inhibitors and glucocorticoids. Overall, HCoV-EMC and SARS-CoV elicit distinct host gene expression responses, which might impact in vivo pathogenesis and could orient therapeutic strategies against that emergent virus.
DOI: 10.1128/mBio.00165-13
PubMed: 23631916
Affiliations:
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Katze</name></author></analytic><series><title level="j">mBio</title><idno type="eISSN">2150-7511</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Line</term><term>Coronavirus (isolation & purification)</term><term>Coronavirus (pathogenicity)</term><term>Coronavirus (physiology)</term><term>Epithelial Cells (immunology)</term><term>Epithelial Cells (virology)</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Immune Tolerance</term><term>Severe Acute Respiratory Syndrome (virology)</term><term>Transcriptome</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Cellules épithéliales (immunologie)</term><term>Cellules épithéliales (virologie)</term><term>Coronavirus (isolement et purification)</term><term>Coronavirus (pathogénicité)</term><term>Coronavirus (physiologie)</term><term>Humains</term><term>Interactions hôte-pathogène</term><term>Lignée cellulaire</term><term>Réplication virale</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Tolérance immunitaire</term><term>Transcriptome</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules épithéliales</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Epithelial Cells</term></keywords><keywords scheme="MESH" qualifier="isolation & purification" xml:lang="en"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="isolement et purification" xml:lang="fr"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Cellules épithéliales</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Epithelial Cells</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Immune Tolerance</term><term>Transcriptome</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Humains</term><term>Interactions hôte-pathogène</term><term>Lignée cellulaire</term><term>Réplication virale</term><term>Tolérance immunitaire</term><term>Transcriptome</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A novel human coronavirus (HCoV-EMC) was recently identified in the Middle East as the causative agent of a severe acute respiratory syndrome (SARS) resembling the illness caused by SARS coronavirus (SARS-CoV). Although derived from the CoV family, the two viruses are genetically distinct and do not use the same receptor. Here, we investigated whether HCoV-EMC and SARS-CoV induce similar or distinct host responses after infection of a human lung epithelial cell line. HCoV-EMC was able to replicate as efficiently as SARS-CoV in Calu-3 cells and similarly induced minimal transcriptomic changes before 12 h postinfection. Later in infection, HCoV-EMC induced a massive dysregulation of the host transcriptome, to a much greater extent than SARS-CoV. Both viruses induced a similar activation of pattern recognition receptors and the interleukin 17 (IL-17) pathway, but HCoV-EMC specifically down-regulated the expression of several genes within the antigen presentation pathway, including both type I and II major histocompatibility complex (MHC) genes. This could have an important impact on the ability of the host to mount an adaptive host response. A unique set of 207 genes was dysregulated early and permanently throughout infection with HCoV-EMC, and was used in a computational screen to predict potential antiviral compounds, including kinase inhibitors and glucocorticoids. Overall, HCoV-EMC and SARS-CoV elicit distinct host gene expression responses, which might impact in vivo pathogenesis and could orient therapeutic strategies against that emergent virus.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23631916</PMID><DateCompleted><Year>2013</Year><Month>11</Month><Day>26</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>04</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2150-7511</ISSN><JournalIssue CitedMedium="Internet"><Volume>4</Volume><Issue>3</Issue><PubDate><Year>2013</Year><Month>Apr</Month><Day>30</Day></PubDate></JournalIssue><Title>mBio</Title><ISOAbbreviation>mBio</ISOAbbreviation></Journal><ArticleTitle>Cell host response to infection with novel human coronavirus EMC predicts potential antivirals and important differences with SARS coronavirus.</ArticleTitle><Pagination><MedlinePgn>e00165-13</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/mBio.00165-13</ELocationID><ELocationID EIdType="pii" ValidYN="Y">e00165-13</ELocationID><Abstract><AbstractText Label="UNLABELLED">A novel human coronavirus (HCoV-EMC) was recently identified in the Middle East as the causative agent of a severe acute respiratory syndrome (SARS) resembling the illness caused by SARS coronavirus (SARS-CoV). Although derived from the CoV family, the two viruses are genetically distinct and do not use the same receptor. Here, we investigated whether HCoV-EMC and SARS-CoV induce similar or distinct host responses after infection of a human lung epithelial cell line. HCoV-EMC was able to replicate as efficiently as SARS-CoV in Calu-3 cells and similarly induced minimal transcriptomic changes before 12 h postinfection. Later in infection, HCoV-EMC induced a massive dysregulation of the host transcriptome, to a much greater extent than SARS-CoV. Both viruses induced a similar activation of pattern recognition receptors and the interleukin 17 (IL-17) pathway, but HCoV-EMC specifically down-regulated the expression of several genes within the antigen presentation pathway, including both type I and II major histocompatibility complex (MHC) genes. This could have an important impact on the ability of the host to mount an adaptive host response. A unique set of 207 genes was dysregulated early and permanently throughout infection with HCoV-EMC, and was used in a computational screen to predict potential antiviral compounds, including kinase inhibitors and glucocorticoids. Overall, HCoV-EMC and SARS-CoV elicit distinct host gene expression responses, which might impact in vivo pathogenesis and could orient therapeutic strategies against that emergent virus.</AbstractText><AbstractText Label="IMPORTANCE" NlmCategory="OBJECTIVE">Identification of a novel coronavirus causing fatal respiratory infection in humans raises concerns about a possible widespread outbreak of severe respiratory infection similar to the one caused by SARS-CoV. Using a human lung epithelial cell line and global transcriptomic profiling, we identified differences in the host response between HCoV-EMC and SARS-CoV. This enables rapid assessment of viral properties and the ability to anticipate possible differences in human clinical responses to HCoV-EMC and SARS-CoV. We used this information to predict potential effective drugs against HCoV-EMC, a method that could be more generally used to identify candidate therapeutics in future disease outbreaks. These data will help to generate hypotheses and make rapid advancements in characterizing this new virus.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Josset</LastName><ForeName>Laurence</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Microbiology, School of Medicine, University of Washington, Seattle, Washington, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Menachery</LastName><ForeName>Vineet D</ForeName><Initials>VD</Initials></Author><Author ValidYN="Y"><LastName>Gralinski</LastName><ForeName>Lisa E</ForeName><Initials>LE</Initials></Author><Author ValidYN="Y"><LastName>Agnihothram</LastName><ForeName>Sudhakar</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Sova</LastName><ForeName>Pavel</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Carter</LastName><ForeName>Victoria S</ForeName><Initials>VS</Initials></Author><Author ValidYN="Y"><LastName>Yount</LastName><ForeName>Boyd L</ForeName><Initials>BL</Initials></Author><Author ValidYN="Y"><LastName>Graham</LastName><ForeName>Rachel L</ForeName><Initials>RL</Initials></Author><Author ValidYN="Y"><LastName>Baric</LastName><ForeName>Ralph S</ForeName><Initials>RS</Initials></Author><Author ValidYN="Y"><LastName>Katze</LastName><ForeName>Michael G</ForeName><Initials>MG</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HHSN272200800060C</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U19 AI100625</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U54 AI081680</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U54AI081680</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>04</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>mBio</MedlineTA><NlmUniqueID>101519231</NlmUniqueID></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017934" MajorTopicYN="N">Coronavirus</DescriptorName><QualifierName UI="Q000302" MajorTopicYN="N">isolation & purification</QualifierName><QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054884" MajorTopicYN="Y">Host-Pathogen Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007108" MajorTopicYN="N">Immune Tolerance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059467" MajorTopicYN="N">Transcriptome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>5</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>5</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>12</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23631916</ArticleId><ArticleId IdType="pii">mBio.00165-13</ArticleId><ArticleId IdType="doi">10.1128/mBio.00165-13</ArticleId><ArticleId IdType="pmc">PMC3663187</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>J Immunol. 2009 Oct 15;183(8):5301-10</Citation><ArticleIdList><ArticleId IdType="pubmed">19783685</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 2003 May;77(10):5649-56</Citation><ArticleIdList><ArticleId IdType="pubmed">12719557</ArticleId></ArticleIdList></Reference><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1967-76</Citation><ArticleIdList><ArticleId IdType="pubmed">12690091</ArticleId></ArticleIdList></Reference><Reference><Citation>Immunology. 2003 Oct;110(2):163-9</Citation><ArticleIdList><ArticleId IdType="pubmed">14511229</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12995-3000</Citation><ArticleIdList><ArticleId IdType="pubmed">14569023</ArticleId></ArticleIdList></Reference><Reference><Citation>N Engl J Med. 2003 Dec 18;349(25):2431-41</Citation><ArticleIdList><ArticleId IdType="pubmed">14681510</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 1996 Nov 29;271(48):30864-9</Citation><ArticleIdList><ArticleId IdType="pubmed">8940070</ArticleId></ArticleIdList></Reference><Reference><Citation>Immunology. 1997 Jul;91(3):458-63</Citation><ArticleIdList><ArticleId IdType="pubmed">9301537</ArticleId></ArticleIdList></Reference><Reference><Citation>J Exp Med. 1998 Jan 5;187(1):97-104</Citation><ArticleIdList><ArticleId IdType="pubmed">9419215</ArticleId></ArticleIdList></Reference><Reference><Citation>J Gen Virol. 2005 Feb;86(Pt 2):375-84</Citation><ArticleIdList><ArticleId IdType="pubmed">15659757</ArticleId></ArticleIdList></Reference><Reference><Citation>Ann Rheum Dis. 2006 Nov;65 Suppl 3:iii83-8</Citation><ArticleIdList><ArticleId IdType="pubmed">17038480</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS Med. 2006 Sep;3(9):e343</Citation><ArticleIdList><ArticleId IdType="pubmed">16968120</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Cancer. 2007 Jan;7(1):54-60</Citation><ArticleIdList><ArticleId IdType="pubmed">17186018</ArticleId></ArticleIdList></Reference><Reference><Citation>J Gen Virol. 2007 Mar;88(Pt 3):942-50</Citation><ArticleIdList><ArticleId IdType="pubmed">17325368</ArticleId></ArticleIdList></Reference><Reference><Citation>BMC Genomics. 2009;10:22</Citation><ArticleIdList><ArticleId IdType="pubmed">19144180</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 2009 Jul;83(13):6883-99</Citation><ArticleIdList><ArticleId IdType="pubmed">19386722</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Immunol. 2009 Jul;9(7):503-13</Citation><ArticleIdList><ArticleId IdType="pubmed">19498380</ArticleId></ArticleIdList></Reference><Reference><Citation>Protein Cell. 2013 Apr;4(4):248-50</Citation><ArticleIdList><ArticleId IdType="pubmed">23549610</ArticleId></ArticleIdList></Reference><Reference><Citation>Expert Opin Biol Ther. 2009 Nov;9(11):1369-82</Citation><ArticleIdList><ArticleId IdType="pubmed">19732026</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Microbiol. 2013 Jul;15(7):1198-211</Citation><ArticleIdList><ArticleId IdType="pubmed">23320394</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS One. 2010;5(1):e8729</Citation><ArticleIdList><ArticleId IdType="pubmed">20090954</ArticleId></ArticleIdList></Reference><Reference><Citation>Eur J Pharmacol. 2010 Jun 10;635(1-3):212-8</Citation><ArticleIdList><ArticleId IdType="pubmed">20226180</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS One. 2010;5(10). pii: e13169. doi: 10.1371/journal.pone.0013169</Citation><ArticleIdList><ArticleId IdType="pubmed">20957181</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol Methods. 2011 Jun;174(1-2):144-9</Citation><ArticleIdList><ArticleId IdType="pubmed">21458491</ArticleId></ArticleIdList></Reference><Reference><Citation>Sci Transl Med. 2011 Aug 17;3(96):96ra77</Citation><ArticleIdList><ArticleId IdType="pubmed">21849665</ArticleId></ArticleIdList></Reference><Reference><Citation>Biol Chem. 2011 Oct;392(10):837-47</Citation><ArticleIdList><ArticleId IdType="pubmed">21823902</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 2011 Nov;85(21):10955-67</Citation><ArticleIdList><ArticleId IdType="pubmed">21865398</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS Pathog. 2011 Oct;7(10):e1002331</Citation><ArticleIdList><ArticleId IdType="pubmed">22046132</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2011 Nov 15;187(10):5357-62</Citation><ArticleIdList><ArticleId IdType="pubmed">21964025</ArticleId></ArticleIdList></Reference><Reference><Citation>J Med Chem. 2011 Nov 24;54(22):7797-814</Citation><ArticleIdList><ArticleId IdType="pubmed">21888439</ArticleId></ArticleIdList></Reference><Reference><Citation>Microbiol Mol Biol Rev. 2012 Mar;76(1):16-32</Citation><ArticleIdList><ArticleId IdType="pubmed">22390970</ArticleId></ArticleIdList></Reference><Reference><Citation>Microbiol Mol Biol Rev. 2012 Mar;76(1):33-45</Citation><ArticleIdList><ArticleId IdType="pubmed">22390971</ArticleId></ArticleIdList></Reference><Reference><Citation>Virus Res. 2012 Apr;165(1):112-7</Citation><ArticleIdList><ArticleId IdType="pubmed">22349148</ArticleId></ArticleIdList></Reference><Reference><Citation>Trends Immunol. 2012 Jul;33(7):343-9</Citation><ArticleIdList><ArticleId IdType="pubmed">22476048</ArticleId></ArticleIdList></Reference><Reference><Citation>Euro Surveill. 2012;17(40):20290</Citation><ArticleIdList><ArticleId IdType="pubmed">23078800</ArticleId></ArticleIdList></Reference><Reference><Citation>N Engl J Med. 2012 Nov 8;367(19):1814-20</Citation><ArticleIdList><ArticleId IdType="pubmed">23075143</ArticleId></ArticleIdList></Reference><Reference><Citation>MBio. 2012;3(6). pii: e00473-12. doi: 10.1128/mBio.00473-12</Citation><ArticleIdList><ArticleId IdType="pubmed">23170002</ArticleId></ArticleIdList></Reference><Reference><Citation>MBio. 2012;3(6). pii: e00515-12. doi: 10.1128/mBio.00515-12</Citation><ArticleIdList><ArticleId IdType="pubmed">23232719</ArticleId></ArticleIdList></Reference><Reference><Citation>Eur J Pharmacol. 2013 Jan 5;698(1-3):455-62</Citation><ArticleIdList><ArticleId IdType="pubmed">23183108</ArticleId></ArticleIdList></Reference><Reference><Citation>MBio. 2013;4(1). pii: e00002-13. doi: 10.1128/mBio.00002-13</Citation><ArticleIdList><ArticleId IdType="pubmed">23322635</ArticleId></ArticleIdList></Reference><Reference><Citation>MBio. 2013;4(1):e00611-12</Citation><ArticleIdList><ArticleId IdType="pubmed">23422412</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Clin Oncol. 2013 Mar;10(3):143-53</Citation><ArticleIdList><ArticleId IdType="pubmed">23400000</ArticleId></ArticleIdList></Reference><Reference><Citation>Arch Med Res. 2013 Feb;44(2):93-8</Citation><ArticleIdList><ArticleId IdType="pubmed">23376055</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 2013 Apr;87(7):3885-902</Citation><ArticleIdList><ArticleId IdType="pubmed">23365422</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2013 Mar 14;495(7440):251-4</Citation><ArticleIdList><ArticleId IdType="pubmed">23486063</ArticleId></ArticleIdList></Reference><Reference><Citation>Methods Mol Biol. 2000;132:365-86</Citation><ArticleIdList><ArticleId IdType="pubmed">10547847</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 2001 Jul;75(13):6022-32</Citation><ArticleIdList><ArticleId IdType="pubmed">11390604</ArticleId></ArticleIdList></Reference><Reference><Citation>Methods. 2001 Dec;25(4):402-8</Citation><ArticleIdList><ArticleId IdType="pubmed">11846609</ArticleId></ArticleIdList></Reference><Reference><Citation>Trends Immunol. 2003 May;24(5):278-85</Citation><ArticleIdList><ArticleId IdType="pubmed">12738423</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Washington (État)</li></region><settlement><li>Seattle</li></settlement><orgName><li>Université de Washington</li></orgName></list><tree><noCountry><name sortKey="Agnihothram, Sudhakar" sort="Agnihothram, Sudhakar" uniqKey="Agnihothram S" first="Sudhakar" last="Agnihothram">Sudhakar Agnihothram</name><name sortKey="Baric, Ralph S" sort="Baric, Ralph S" uniqKey="Baric R" first="Ralph S" last="Baric">Ralph S. Baric</name><name sortKey="Carter, Victoria S" sort="Carter, Victoria S" uniqKey="Carter V" first="Victoria S" last="Carter">Victoria S. Carter</name><name sortKey="Graham, Rachel L" sort="Graham, Rachel L" uniqKey="Graham R" first="Rachel L" last="Graham">Rachel L. Graham</name><name sortKey="Gralinski, Lisa E" sort="Gralinski, Lisa E" uniqKey="Gralinski L" first="Lisa E" last="Gralinski">Lisa E. Gralinski</name><name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G" last="Katze">Michael G. Katze</name><name sortKey="Menachery, Vineet D" sort="Menachery, Vineet D" uniqKey="Menachery V" first="Vineet D" last="Menachery">Vineet D. Menachery</name><name sortKey="Sova, Pavel" sort="Sova, Pavel" uniqKey="Sova P" first="Pavel" last="Sova">Pavel Sova</name><name sortKey="Yount, Boyd L" sort="Yount, Boyd L" uniqKey="Yount B" first="Boyd L" last="Yount">Boyd L. Yount</name></noCountry><country name="États-Unis"><region name="Washington (État)"><name sortKey="Josset, Laurence" sort="Josset, Laurence" uniqKey="Josset L" first="Laurence" last="Josset">Laurence Josset</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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