Chemokine up-regulation in SARS-coronavirus-infected, monocyte-derived human dendritic cells.
Identifieur interne : 000F22 ( Ncbi/Merge ); précédent : 000F21; suivant : 000F23Chemokine up-regulation in SARS-coronavirus-infected, monocyte-derived human dendritic cells.
Auteurs : Helen K W. Law [République populaire de Chine] ; Chung Yan Cheung ; Hoi Yee Ng ; Sin Fun Sia ; Yuk On Chan ; Winsie Luk ; John M. Nicholls ; J S Malik Peiris ; Yu Lung LauSource :
- Blood [ 0006-4971 ] ; 2005.
Descripteurs français
- KwdFr :
- ARN (métabolisme), ARN viral (métabolisme), Activation enzymatique, Agranulocytes (cytologie), Amorces ADN (), Apoptose, Caspase-3, Caspases (biosynthèse), Cellules cultivées, Cellules dendritiques (cytologie), Chimiokine CCL2 (biosynthèse), Chimiokine CCL3, Chimiokine CCL4, Chimiokine CCL5 (biosynthèse), Chimiokines (biosynthèse), Cytokines (métabolisme), Cytométrie en flux, Facteurs temps, Humains, Inflammation, Interféron alpha (biosynthèse), Interféron bêta (biosynthèse), Interféron gamma (biosynthèse), Interleukine-12 (biosynthèse), Interleukine-12 (métabolisme), Interleukine-6 (biosynthèse), Microscopie de fluorescence, Microscopie électronique à transmission, Monocytes (cytologie), Protéines inflammatoires des macrophages (biosynthèse), RT-PCR, Réaction de polymérisation en chaîne, Régulation positive, Sous-unité p40 de l'interleukine-12, Sous-unités de protéines (biosynthèse), Séparation cellulaire, Technique d'immunofluorescence indirecte, Virus du SRAS (génétique), Virus du SRAS (métabolisme).
- MESH :
- biosynthèse : Caspases, Chimiokine CCL2, Chimiokine CCL5, Chimiokines, Interféron alpha, Interféron bêta, Interféron gamma, Interleukine-12, Interleukine-6, Protéines inflammatoires des macrophages, Sous-unités de protéines.
- cytologie : Agranulocytes, Cellules dendritiques, Monocytes.
- génétique : Virus du SRAS.
- métabolisme : ARN, ARN viral, Cytokines, Interleukine-12, Virus du SRAS.
- Activation enzymatique, Amorces ADN, Apoptose, Caspase-3, Cellules cultivées, Chimiokine CCL3, Chimiokine CCL4, Cytométrie en flux, Facteurs temps, Humains, Inflammation, Microscopie de fluorescence, Microscopie électronique à transmission, RT-PCR, Réaction de polymérisation en chaîne, Régulation positive, Sous-unité p40 de l'interleukine-12, Séparation cellulaire, Technique d'immunofluorescence indirecte.
English descriptors
- KwdEn :
- Apoptosis, Caspase 3, Caspases (biosynthesis), Cell Separation, Cells, Cultured, Chemokine CCL2 (biosynthesis), Chemokine CCL3, Chemokine CCL4, Chemokine CCL5 (biosynthesis), Chemokines (biosynthesis), Cytokines (metabolism), DNA Primers (chemistry), Dendritic Cells (cytology), Enzyme Activation, Flow Cytometry, Fluorescent Antibody Technique, Indirect, Humans, Inflammation, Interferon-alpha (biosynthesis), Interferon-beta (biosynthesis), Interferon-gamma (biosynthesis), Interleukin-12 (biosynthesis), Interleukin-12 (metabolism), Interleukin-12 Subunit p40, Interleukin-6 (biosynthesis), Leukocytes, Mononuclear (cytology), Macrophage Inflammatory Proteins (biosynthesis), Microscopy, Electron, Transmission, Microscopy, Fluorescence, Monocytes (cytology), Polymerase Chain Reaction, Protein Subunits (biosynthesis), RNA (metabolism), RNA, Viral (metabolism), Reverse Transcriptase Polymerase Chain Reaction, SARS Virus (genetics), SARS Virus (metabolism), Time Factors, Up-Regulation.
- MESH :
- chemical , biosynthesis : Caspases, Chemokine CCL2, Chemokine CCL5, Chemokines, Interferon-alpha, Interferon-beta, Interferon-gamma, Interleukin-12, Interleukin-6, Macrophage Inflammatory Proteins, Protein Subunits.
- chemical , chemistry : DNA Primers.
- chemical , metabolism : Cytokines, Interleukin-12, RNA, RNA, Viral.
- chemical : Caspase 3, Chemokine CCL3, Chemokine CCL4, Interleukin-12 Subunit p40.
- cytology : Dendritic Cells, Leukocytes, Mononuclear, Monocytes.
- genetics : SARS Virus.
- metabolism : SARS Virus.
- Apoptosis, Cell Separation, Cells, Cultured, Enzyme Activation, Flow Cytometry, Fluorescent Antibody Technique, Indirect, Humans, Inflammation, Microscopy, Electron, Transmission, Microscopy, Fluorescence, Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Time Factors, Up-Regulation.
Abstract
Lymphopenia and increasing viral load in the first 10 days of severe acute respiratory syndrome (SARS) suggested immune evasion by SARS-coronavirus (CoV). In this study, we focused on dendritic cells (DCs) which play important roles in linking the innate and adaptive immunity. SARS-CoV was shown to infect both immature and mature human monocyte-derived DCs by electron microscopy and immunofluorescence. The detection of negative strands of SARS-CoV RNA in DCs suggested viral replication. However, no increase in viral RNA was observed. Using cytopathic assays, no increase in virus titer was detected in infected DCs and cell-culture supernatant, confirming that virus replication was incomplete. No induction of apoptosis or maturation was detected in SARS-CoV-infected DCs. The SARS-CoV-infected DCs showed low expression of antiviral cytokines (interferon alpha [IFN-alpha], IFN-beta, IFN-gamma, and interleukin 12p40 [IL-12p40]), moderate up-regulation of proinflammatory cytokines (tumor necrosis factor alpha [TNF-alpha] and IL-6) but significant up-regulation of inflammatory chemokines (macrophage inflammatory protein 1alpha [MIP-1alpha], regulated on activation normal T cell expressed and secreted [RANTES]), interferon-inducible protein of 10 kDa [IP-10], and monocyte chemoattractant protein 1 [MCP-1]). The lack of antiviral cytokine response against a background of intense chemokine up-regulation could represent a mechanism of immune evasion by SARS-CoV.
DOI: 10.1182/blood-2004-10-4166
PubMed: 15860669
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 002764
- to stream PubMed, to step Curation: 002764
- to stream PubMed, to step Checkpoint: 002798
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pubmed:15860669Le document en format XML
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Law</name><affiliation wicri:level="1"><nlm:affiliation>Department of Paediatrics and Adolescent Medicine, Hong Kong Jockey Club Clinical Research Centre, Faculty of Medicine, The University of Hong Kong, Queen Mary Hospital, Pokfulam, Hong Kong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Paediatrics and Adolescent Medicine, Hong Kong Jockey Club Clinical Research Centre, Faculty of Medicine, The University of Hong Kong, Queen Mary Hospital, Pokfulam, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Cheung, Chung Yan" sort="Cheung, Chung Yan" uniqKey="Cheung C" first="Chung Yan" last="Cheung">Chung Yan Cheung</name></author><author><name sortKey="Ng, Hoi Yee" sort="Ng, Hoi Yee" uniqKey="Ng H" first="Hoi Yee" last="Ng">Hoi Yee Ng</name></author><author><name sortKey="Sia, Sin Fun" sort="Sia, Sin Fun" uniqKey="Sia S" first="Sin Fun" last="Sia">Sin Fun Sia</name></author><author><name sortKey="Chan, Yuk On" sort="Chan, Yuk On" uniqKey="Chan Y" first="Yuk On" last="Chan">Yuk On Chan</name></author><author><name sortKey="Luk, Winsie" sort="Luk, Winsie" uniqKey="Luk W" first="Winsie" last="Luk">Winsie Luk</name></author><author><name sortKey="Nicholls, John M" sort="Nicholls, John M" uniqKey="Nicholls J" first="John M" last="Nicholls">John M. 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Law</name><affiliation wicri:level="1"><nlm:affiliation>Department of Paediatrics and Adolescent Medicine, Hong Kong Jockey Club Clinical Research Centre, Faculty of Medicine, The University of Hong Kong, Queen Mary Hospital, Pokfulam, Hong Kong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Paediatrics and Adolescent Medicine, Hong Kong Jockey Club Clinical Research Centre, Faculty of Medicine, The University of Hong Kong, Queen Mary Hospital, Pokfulam, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Cheung, Chung Yan" sort="Cheung, Chung Yan" uniqKey="Cheung C" first="Chung Yan" last="Cheung">Chung Yan Cheung</name></author><author><name sortKey="Ng, Hoi Yee" sort="Ng, Hoi Yee" uniqKey="Ng H" first="Hoi Yee" last="Ng">Hoi Yee Ng</name></author><author><name sortKey="Sia, Sin Fun" sort="Sia, Sin Fun" uniqKey="Sia S" first="Sin Fun" last="Sia">Sin Fun Sia</name></author><author><name sortKey="Chan, Yuk On" sort="Chan, Yuk On" uniqKey="Chan Y" first="Yuk On" last="Chan">Yuk On Chan</name></author><author><name sortKey="Luk, Winsie" sort="Luk, Winsie" uniqKey="Luk W" first="Winsie" last="Luk">Winsie Luk</name></author><author><name sortKey="Nicholls, John M" sort="Nicholls, John M" uniqKey="Nicholls J" first="John M" last="Nicholls">John M. Nicholls</name></author><author><name sortKey="Peiris, J S Malik" sort="Peiris, J S Malik" uniqKey="Peiris J" first="J S Malik" last="Peiris">J S Malik Peiris</name></author><author><name sortKey="Lau, Yu Lung" sort="Lau, Yu Lung" uniqKey="Lau Y" first="Yu Lung" last="Lau">Yu Lung Lau</name></author></analytic><series><title level="j">Blood</title><idno type="ISSN">0006-4971</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis</term><term>Caspase 3</term><term>Caspases (biosynthesis)</term><term>Cell Separation</term><term>Cells, Cultured</term><term>Chemokine CCL2 (biosynthesis)</term><term>Chemokine CCL3</term><term>Chemokine CCL4</term><term>Chemokine CCL5 (biosynthesis)</term><term>Chemokines (biosynthesis)</term><term>Cytokines (metabolism)</term><term>DNA Primers (chemistry)</term><term>Dendritic Cells (cytology)</term><term>Enzyme Activation</term><term>Flow Cytometry</term><term>Fluorescent Antibody Technique, Indirect</term><term>Humans</term><term>Inflammation</term><term>Interferon-alpha (biosynthesis)</term><term>Interferon-beta (biosynthesis)</term><term>Interferon-gamma (biosynthesis)</term><term>Interleukin-12 (biosynthesis)</term><term>Interleukin-12 (metabolism)</term><term>Interleukin-12 Subunit p40</term><term>Interleukin-6 (biosynthesis)</term><term>Leukocytes, Mononuclear (cytology)</term><term>Macrophage Inflammatory Proteins (biosynthesis)</term><term>Microscopy, Electron, Transmission</term><term>Microscopy, Fluorescence</term><term>Monocytes (cytology)</term><term>Polymerase Chain Reaction</term><term>Protein Subunits (biosynthesis)</term><term>RNA (metabolism)</term><term>RNA, Viral (metabolism)</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>SARS Virus (genetics)</term><term>SARS Virus (metabolism)</term><term>Time Factors</term><term>Up-Regulation</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN (métabolisme)</term><term>ARN viral (métabolisme)</term><term>Activation enzymatique</term><term>Agranulocytes (cytologie)</term><term>Amorces ADN ()</term><term>Apoptose</term><term>Caspase-3</term><term>Caspases (biosynthèse)</term><term>Cellules cultivées</term><term>Cellules dendritiques (cytologie)</term><term>Chimiokine CCL2 (biosynthèse)</term><term>Chimiokine CCL3</term><term>Chimiokine CCL4</term><term>Chimiokine CCL5 (biosynthèse)</term><term>Chimiokines (biosynthèse)</term><term>Cytokines (métabolisme)</term><term>Cytométrie en flux</term><term>Facteurs temps</term><term>Humains</term><term>Inflammation</term><term>Interféron alpha (biosynthèse)</term><term>Interféron bêta (biosynthèse)</term><term>Interféron gamma (biosynthèse)</term><term>Interleukine-12 (biosynthèse)</term><term>Interleukine-12 (métabolisme)</term><term>Interleukine-6 (biosynthèse)</term><term>Microscopie de fluorescence</term><term>Microscopie électronique à transmission</term><term>Monocytes (cytologie)</term><term>Protéines inflammatoires des macrophages (biosynthèse)</term><term>RT-PCR</term><term>Réaction de polymérisation en chaîne</term><term>Régulation positive</term><term>Sous-unité p40 de l'interleukine-12</term><term>Sous-unités de protéines (biosynthèse)</term><term>Séparation cellulaire</term><term>Technique d'immunofluorescence indirecte</term><term>Virus du SRAS (génétique)</term><term>Virus du SRAS (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Caspases</term><term>Chemokine CCL2</term><term>Chemokine CCL5</term><term>Chemokines</term><term>Interferon-alpha</term><term>Interferon-beta</term><term>Interferon-gamma</term><term>Interleukin-12</term><term>Interleukin-6</term><term>Macrophage Inflammatory Proteins</term><term>Protein Subunits</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>DNA Primers</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>Interleukin-12</term><term>RNA</term><term>RNA, Viral</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Caspase 3</term><term>Chemokine CCL3</term><term>Chemokine CCL4</term><term>Interleukin-12 Subunit p40</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Caspases</term><term>Chimiokine CCL2</term><term>Chimiokine CCL5</term><term>Chimiokines</term><term>Interféron alpha</term><term>Interféron bêta</term><term>Interféron gamma</term><term>Interleukine-12</term><term>Interleukine-6</term><term>Protéines inflammatoires des macrophages</term><term>Sous-unités de protéines</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Agranulocytes</term><term>Cellules dendritiques</term><term>Monocytes</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Dendritic Cells</term><term>Leukocytes, Mononuclear</term><term>Monocytes</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN</term><term>ARN viral</term><term>Cytokines</term><term>Interleukine-12</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Apoptosis</term><term>Cell Separation</term><term>Cells, Cultured</term><term>Enzyme Activation</term><term>Flow Cytometry</term><term>Fluorescent Antibody Technique, Indirect</term><term>Humans</term><term>Inflammation</term><term>Microscopy, Electron, Transmission</term><term>Microscopy, Fluorescence</term><term>Polymerase Chain Reaction</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Time Factors</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Activation enzymatique</term><term>Amorces ADN</term><term>Apoptose</term><term>Caspase-3</term><term>Cellules cultivées</term><term>Chimiokine CCL3</term><term>Chimiokine CCL4</term><term>Cytométrie en flux</term><term>Facteurs temps</term><term>Humains</term><term>Inflammation</term><term>Microscopie de fluorescence</term><term>Microscopie électronique à transmission</term><term>RT-PCR</term><term>Réaction de polymérisation en chaîne</term><term>Régulation positive</term><term>Sous-unité p40 de l'interleukine-12</term><term>Séparation cellulaire</term><term>Technique d'immunofluorescence indirecte</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lymphopenia and increasing viral load in the first 10 days of severe acute respiratory syndrome (SARS) suggested immune evasion by SARS-coronavirus (CoV). In this study, we focused on dendritic cells (DCs) which play important roles in linking the innate and adaptive immunity. SARS-CoV was shown to infect both immature and mature human monocyte-derived DCs by electron microscopy and immunofluorescence. The detection of negative strands of SARS-CoV RNA in DCs suggested viral replication. However, no increase in viral RNA was observed. Using cytopathic assays, no increase in virus titer was detected in infected DCs and cell-culture supernatant, confirming that virus replication was incomplete. No induction of apoptosis or maturation was detected in SARS-CoV-infected DCs. The SARS-CoV-infected DCs showed low expression of antiviral cytokines (interferon alpha [IFN-alpha], IFN-beta, IFN-gamma, and interleukin 12p40 [IL-12p40]), moderate up-regulation of proinflammatory cytokines (tumor necrosis factor alpha [TNF-alpha] and IL-6) but significant up-regulation of inflammatory chemokines (macrophage inflammatory protein 1alpha [MIP-1alpha], regulated on activation normal T cell expressed and secreted [RANTES]), interferon-inducible protein of 10 kDa [IP-10], and monocyte chemoattractant protein 1 [MCP-1]). The lack of antiviral cytokine response against a background of intense chemokine up-regulation could represent a mechanism of immune evasion by SARS-CoV.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15860669</PMID><DateCompleted><Year>2005</Year><Month>11</Month><Day>28</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0006-4971</ISSN><JournalIssue CitedMedium="Print"><Volume>106</Volume><Issue>7</Issue><PubDate><Year>2005</Year><Month>Oct</Month><Day>01</Day></PubDate></JournalIssue><Title>Blood</Title><ISOAbbreviation>Blood</ISOAbbreviation></Journal><ArticleTitle>Chemokine up-regulation in SARS-coronavirus-infected, monocyte-derived human dendritic cells.</ArticleTitle><Pagination><MedlinePgn>2366-74</MedlinePgn></Pagination><Abstract><AbstractText>Lymphopenia and increasing viral load in the first 10 days of severe acute respiratory syndrome (SARS) suggested immune evasion by SARS-coronavirus (CoV). In this study, we focused on dendritic cells (DCs) which play important roles in linking the innate and adaptive immunity. SARS-CoV was shown to infect both immature and mature human monocyte-derived DCs by electron microscopy and immunofluorescence. The detection of negative strands of SARS-CoV RNA in DCs suggested viral replication. However, no increase in viral RNA was observed. Using cytopathic assays, no increase in virus titer was detected in infected DCs and cell-culture supernatant, confirming that virus replication was incomplete. No induction of apoptosis or maturation was detected in SARS-CoV-infected DCs. The SARS-CoV-infected DCs showed low expression of antiviral cytokines (interferon alpha [IFN-alpha], IFN-beta, IFN-gamma, and interleukin 12p40 [IL-12p40]), moderate up-regulation of proinflammatory cytokines (tumor necrosis factor alpha [TNF-alpha] and IL-6) but significant up-regulation of inflammatory chemokines (macrophage inflammatory protein 1alpha [MIP-1alpha], regulated on activation normal T cell expressed and secreted [RANTES]), interferon-inducible protein of 10 kDa [IP-10], and monocyte chemoattractant protein 1 [MCP-1]). The lack of antiviral cytokine response against a background of intense chemokine up-regulation could represent a mechanism of immune evasion by SARS-CoV.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Law</LastName><ForeName>Helen K W</ForeName><Initials>HK</Initials><AffiliationInfo><Affiliation>Department of Paediatrics and Adolescent Medicine, Hong Kong Jockey Club Clinical Research Centre, Faculty of Medicine, The University of Hong Kong, Queen Mary Hospital, Pokfulam, Hong Kong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheung</LastName><ForeName>Chung Yan</ForeName><Initials>CY</Initials></Author><Author ValidYN="Y"><LastName>Ng</LastName><ForeName>Hoi Yee</ForeName><Initials>HY</Initials></Author><Author ValidYN="Y"><LastName>Sia</LastName><ForeName>Sin Fun</ForeName><Initials>SF</Initials></Author><Author ValidYN="Y"><LastName>Chan</LastName><ForeName>Yuk On</ForeName><Initials>YO</Initials></Author><Author ValidYN="Y"><LastName>Luk</LastName><ForeName>Winsie</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Nicholls</LastName><ForeName>John M</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Peiris</LastName><ForeName>J S Malik</ForeName><Initials>JS</Initials></Author><Author ValidYN="Y"><LastName>Lau</LastName><ForeName>Yu Lung</ForeName><Initials>YL</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AI95357</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2005</Year><Month>04</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Blood</MedlineTA><NlmUniqueID>7603509</NlmUniqueID><ISSNLinking>0006-4971</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018932">Chemokine CCL2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054405">Chemokine CCL3</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054407">Chemokine CCL4</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018946">Chemokine CCL5</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018925">Chemokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017931">DNA Primers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016898">Interferon-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053762">Interleukin-12 Subunit p40</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015850">Interleukin-6</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019402">Macrophage Inflammatory Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D021122">Protein Subunits</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012367">RNA, Viral</NameOfSubstance></Chemical><Chemical><RegistryNumber>187348-17-0</RegistryNumber><NameOfSubstance 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Nicholls</name><name sortKey="Peiris, J S Malik" sort="Peiris, J S Malik" uniqKey="Peiris J" first="J S Malik" last="Peiris">J S Malik Peiris</name><name sortKey="Sia, Sin Fun" sort="Sia, Sin Fun" uniqKey="Sia S" first="Sin Fun" last="Sia">Sin Fun Sia</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Law, Helen K W" sort="Law, Helen K W" uniqKey="Law H" first="Helen K W" last="Law">Helen K W. Law</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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