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Article: Chemokine up-regulation in SARS-coronavirus-infected, monocyte-derived human dendritic cells

TitleChemokine up-regulation in SARS-coronavirus-infected, monocyte-derived human dendritic cells
Authors
Issue Date2005
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
Citation
Blood, 2005, v. 106 n. 7, p. 2366-2374 How to Cite?
AbstractLymphopenia 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 α [IFN-α], IFN-β, IFN-γ, and interleukin 12p40 [IL-12p40]), moderate up-regulation of proinflammatory cytokines (tumor necrosis factor α [TNF-α] and IL-6) but significant up-regulation of inflammatory chemokines (macrophage inflammatory protein 1α [MIP-1α], 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 upregulation could represent a mechanism of immune evasion by SARS-CoV. © 2005 by The American Society of Hematology.
Persistent Identifierhttp://hdl.handle.net/10722/48636
ISSN
2015 Impact Factor: 11.841
2015 SCImago Journal Rankings: 6.395
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLaw, HKWen_HK
dc.contributor.authorChung, YCen_HK
dc.contributor.authorHoi, YNen_HK
dc.contributor.authorSin, FSen_HK
dc.contributor.authorYuk, OCen_HK
dc.contributor.authorLuk, Wen_HK
dc.contributor.authorNicholls, JMen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.contributor.authorLau, YLen_HK
dc.date.accessioned2008-05-22T04:19:41Z-
dc.date.available2008-05-22T04:19:41Z-
dc.date.issued2005en_HK
dc.identifier.citationBlood, 2005, v. 106 n. 7, p. 2366-2374en_HK
dc.identifier.issn0006-4971en_HK
dc.identifier.urihttp://hdl.handle.net/10722/48636-
dc.description.abstractLymphopenia 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 α [IFN-α], IFN-β, IFN-γ, and interleukin 12p40 [IL-12p40]), moderate up-regulation of proinflammatory cytokines (tumor necrosis factor α [TNF-α] and IL-6) but significant up-regulation of inflammatory chemokines (macrophage inflammatory protein 1α [MIP-1α], 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 upregulation could represent a mechanism of immune evasion by SARS-CoV. © 2005 by The American Society of Hematology.en_HK
dc.format.extent1048366 bytes-
dc.format.extent4956 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypetext/plain-
dc.languageengen_HK
dc.publisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/en_HK
dc.relation.ispartofBlooden_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshInterleukin-12 - biosynthesis - metabolismen_HK
dc.subject.meshLeukocytes, Mononuclear - cytologyen_HK
dc.subject.meshUp-Regulationen_HK
dc.subject.meshSARS Virus - genetics - metabolismen_HK
dc.subject.meshMonocytes - cytologyen_HK
dc.titleChemokine up-regulation in SARS-coronavirus-infected, monocyte-derived human dendritic cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-4971&volume=106&issue=7&spage=2366&epage=2374&date=2005&atitle=Chemokine+up-regulation+in+SARS-coronavirus-infected,+monocyte-derived+human+dendritic+cellsen_HK
dc.identifier.emailChung, YC: chungey@hkucc.hku.hken_HK
dc.identifier.emailNicholls, JM: jmnichol@hkucc.hku.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.emailLau, YL: lauylung@hku.hken_HK
dc.identifier.authorityChung, YC=rp00404en_HK
dc.identifier.authorityNicholls, JM=rp00364en_HK
dc.identifier.authorityPeiris, JSM=rp00410en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.description.naturepostprinten_HK
dc.identifier.doi10.1182/blood-2004-10-4166en_HK
dc.identifier.pmid15860669-
dc.identifier.pmcidPMC1895271-
dc.identifier.scopuseid_2-s2.0-27144497805en_HK
dc.identifier.hkuros103548-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-27144497805&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume106en_HK
dc.identifier.issue7en_HK
dc.identifier.spage2366en_HK
dc.identifier.epage2374en_HK
dc.identifier.isiWOS:000232134700031-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLaw, HKW=7101939394en_HK
dc.identifier.scopusauthoridChung, YC=7202061836en_HK
dc.identifier.scopusauthoridHoi, YN=8968426900en_HK
dc.identifier.scopusauthoridSin, FS=8968427000en_HK
dc.identifier.scopusauthoridYuk, OC=8968427100en_HK
dc.identifier.scopusauthoridLuk, W=7005237837en_HK
dc.identifier.scopusauthoridNicholls, JM=7201463077en_HK
dc.identifier.scopusauthoridPeiris, JSM=7005486823en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK

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