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Article: Cytokine responses in severe acute respiratory syndrome coronavirus-infected macrophages in vitro: Possible relevance to pathogenesis

TitleCytokine responses in severe acute respiratory syndrome coronavirus-infected macrophages in vitro: Possible relevance to pathogenesis
Authors
Issue Date2005
PublisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/
Citation
Journal Of Virology, 2005, v. 79 n. 12, p. 7819-7826 How to Cite?
AbstractThe pathogenesis of severe acute respiratory syndrome (SARS) remains unclear. Macrophages are key sentinel cells in the respiratory system, and it is therefore relevant to compare the responses of human macrophages to infections with the SARS coronavirus (SARS-CoV) and other respiratory viruses. Primary human monocyte-derived macrophages were infected with SARS-CoV in vitro. Virus replication was monitored by measuring the levels of positive- and negative-strand RNA, by immunofluorescence detection of the SARS-CoV nucleoprotein, and by titration of the infectious virus. The gene expression profiles of macrophages infected with SARS-CoV, human coronavirus 229E, and influenza A (H1N1) virus were compared by using microarrays and real-time quantitative reverse transcriptase PCR. Secreted cytokines were measured with an enzyme-linked immunosorbent assay. SARS-CoV initiated viral gene transcription and protein synthesis in macrophages, but replication was abortive and no infectious virus was produced. In contrast to the case with human coronavirus 229E and influenza A virus, there was little or no induction of beta interferon (IFN-β) in SARS-CoV-infected macrophages. Furthermore, SARS-CoV induced the expression of chemokines such as CXCL10/IFN-γ-inducible protein 10 and CCL2/monocyte chemotactic protein 1. The poor induction of IFN-β, a key component of innate immunity, and the ability of the virus to induce chemokines could explain aspects of the pathogenesis of SARS. Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/49151
ISSN
2015 Impact Factor: 4.606
2015 SCImago Journal Rankings: 3.347
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, CYen_HK
dc.contributor.authorPoon, LLMen_HK
dc.contributor.authorNg, IHYen_HK
dc.contributor.authorLuk, Wen_HK
dc.contributor.authorSia, SFen_HK
dc.contributor.authorWu, MHSen_HK
dc.contributor.authorChan, KHen_HK
dc.contributor.authorYuen, KYen_HK
dc.contributor.authorGordon, Sen_HK
dc.contributor.authorGuan, Yen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.date.accessioned2008-06-12T06:35:34Z-
dc.date.available2008-06-12T06:35:34Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of Virology, 2005, v. 79 n. 12, p. 7819-7826en_HK
dc.identifier.issn0022-538Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/49151-
dc.description.abstractThe pathogenesis of severe acute respiratory syndrome (SARS) remains unclear. Macrophages are key sentinel cells in the respiratory system, and it is therefore relevant to compare the responses of human macrophages to infections with the SARS coronavirus (SARS-CoV) and other respiratory viruses. Primary human monocyte-derived macrophages were infected with SARS-CoV in vitro. Virus replication was monitored by measuring the levels of positive- and negative-strand RNA, by immunofluorescence detection of the SARS-CoV nucleoprotein, and by titration of the infectious virus. The gene expression profiles of macrophages infected with SARS-CoV, human coronavirus 229E, and influenza A (H1N1) virus were compared by using microarrays and real-time quantitative reverse transcriptase PCR. Secreted cytokines were measured with an enzyme-linked immunosorbent assay. SARS-CoV initiated viral gene transcription and protein synthesis in macrophages, but replication was abortive and no infectious virus was produced. In contrast to the case with human coronavirus 229E and influenza A virus, there was little or no induction of beta interferon (IFN-β) in SARS-CoV-infected macrophages. Furthermore, SARS-CoV induced the expression of chemokines such as CXCL10/IFN-γ-inducible protein 10 and CCL2/monocyte chemotactic protein 1. The poor induction of IFN-β, a key component of innate immunity, and the ability of the virus to induce chemokines could explain aspects of the pathogenesis of SARS. Copyright © 2005, American Society for Microbiology. All Rights Reserved.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/en_HK
dc.relation.ispartofJournal of Virologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsJournal of Virology. Copyright © American Society for Microbiology.en_HK
dc.rightsCopyright © American Society for Microbiology, Journal of Virology, 2005, v. 79 n. 12, p. 7819-7826en_HK
dc.subject.meshCytokines - genetics - metabolismen_HK
dc.subject.meshMacrophages - immunology - virologyen_HK
dc.subject.meshSARS Virus - pathogenicityen_HK
dc.subject.meshSevere Acute Respiratory Syndrome - immunology - virologyen_HK
dc.subject.meshViral Proteins - genetics - metabolismen_HK
dc.titleCytokine responses in severe acute respiratory syndrome coronavirus-infected macrophages in vitro: Possible relevance to pathogenesisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-538X&volume=79&issue=12&spage=7819&epage=7826&date=2005&atitle=Cytokine+responses+in+severe+acute+respiratory+syndrome+coronavirus-infected+macrophages+in+vitro:+possible+relevance+to+pathogenesisen_HK
dc.identifier.emailCheung, CY: chungey@hkucc.hku.hken_HK
dc.identifier.emailPoon, LLM: llmpoon@hkucc.hku.hken_HK
dc.identifier.emailYuen, KY: kyyuen@hkucc.hku.hken_HK
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.authorityCheung, CY=rp00404en_HK
dc.identifier.authorityPoon, LLM=rp00484en_HK
dc.identifier.authorityYuen, KY=rp00366en_HK
dc.identifier.authorityGuan, Y=rp00397en_HK
dc.identifier.authorityPeiris, JSM=rp00410en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1128/JVI.79.12.7819-7826.2005en_HK
dc.identifier.pmid15919935-
dc.identifier.pmcidPMC1143636en_HK
dc.identifier.scopuseid_2-s2.0-19944415600en_HK
dc.identifier.hkuros106321-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-19944415600&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume79en_HK
dc.identifier.issue12en_HK
dc.identifier.spage7819en_HK
dc.identifier.epage7826en_HK
dc.identifier.isiWOS:000229416100054-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheung, CY=7202061836en_HK
dc.identifier.scopusauthoridPoon, LLM=7005441747en_HK
dc.identifier.scopusauthoridNg, IHY=8671050800en_HK
dc.identifier.scopusauthoridLuk, W=7005237837en_HK
dc.identifier.scopusauthoridSia, SF=8574447900en_HK
dc.identifier.scopusauthoridWu, MHS=8574448000en_HK
dc.identifier.scopusauthoridChan, KH=7406034307en_HK
dc.identifier.scopusauthoridYuen, KY=36078079100en_HK
dc.identifier.scopusauthoridGordon, S=35391350600en_HK
dc.identifier.scopusauthoridGuan, Y=7202924055en_HK
dc.identifier.scopusauthoridPeiris, JSM=7005486823en_HK

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