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Article: Comparative host gene transcription by microarray analysis early after infection of the Huh7 cell line by severe acute respiratory syndrome coronavirus and human coronavirus 229E

TitleComparative host gene transcription by microarray analysis early after infection of the Huh7 cell line by severe acute respiratory syndrome coronavirus and human coronavirus 229E
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. 10, p. 6180-6193 How to Cite?
AbstractThe pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) at the cellular level is unclear. No human cell line was previously known to be susceptible to both SARS-CoV and other human coronavinises. Huh7 cells were found to be susceptible to both SARS-CoV, associated with SARS, and human coronavirus 229E (HCoV-229E), usually associated with the common cold. Highly lytic and productive rates of infections within 48 h of inoculation were reproducible with both viruses. The early transcriptional profiles of host cell response to both types of infection at 2 and 4 h postinoculation were determined by using the Affymetrix HG-U133A microarray (about 22,000 genes). Much more perturbation of cellular gene transcription was observed after infection by SARS-CoV than after infection by HCoV-229E. Besides the upregulation of genes associated with apoptosis, which was exactly opposite to the previously reported effect of SARS-CoV in a colonic carcinoma cell line, genes related to inflammation, stress response, and procoagulation were also upregulated. These findings were confirmed by semiquantitative reverse transcription-PCR, reverse transcription-quantitative PCR for mRNA of genes, and immunoassays for some encoded proteins. These transcriptomal changes are compatible with the histological changes of pulmonary vasculitis and microvascular thrombosis in addition to the diffuse alveolar damage involving the pneumocytes. Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/49149
ISSN
2015 Impact Factor: 4.606
2015 SCImago Journal Rankings: 3.347
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, BSFen_HK
dc.contributor.authorChan, KHen_HK
dc.contributor.authorCheng, VCCen_HK
dc.contributor.authorWoo, PCYen_HK
dc.contributor.authorLau, SKPen_HK
dc.contributor.authorLam, CCKen_HK
dc.contributor.authorChan, TLen_HK
dc.contributor.authorWu, AKLen_HK
dc.contributor.authorHung, IFNen_HK
dc.contributor.authorLeung, SYen_HK
dc.contributor.authorYuen, KYen_HK
dc.date.accessioned2008-06-12T06:35:32Z-
dc.date.available2008-06-12T06:35:32Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of Virology, 2005, v. 79 n. 10, p. 6180-6193en_HK
dc.identifier.issn0022-538Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/49149-
dc.description.abstractThe pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) at the cellular level is unclear. No human cell line was previously known to be susceptible to both SARS-CoV and other human coronavinises. Huh7 cells were found to be susceptible to both SARS-CoV, associated with SARS, and human coronavirus 229E (HCoV-229E), usually associated with the common cold. Highly lytic and productive rates of infections within 48 h of inoculation were reproducible with both viruses. The early transcriptional profiles of host cell response to both types of infection at 2 and 4 h postinoculation were determined by using the Affymetrix HG-U133A microarray (about 22,000 genes). Much more perturbation of cellular gene transcription was observed after infection by SARS-CoV than after infection by HCoV-229E. Besides the upregulation of genes associated with apoptosis, which was exactly opposite to the previously reported effect of SARS-CoV in a colonic carcinoma cell line, genes related to inflammation, stress response, and procoagulation were also upregulated. These findings were confirmed by semiquantitative reverse transcription-PCR, reverse transcription-quantitative PCR for mRNA of genes, and immunoassays for some encoded proteins. These transcriptomal changes are compatible with the histological changes of pulmonary vasculitis and microvascular thrombosis in addition to the diffuse alveolar damage involving the pneumocytes. 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.rightsJournal of virology. Copyright © American Society for Microbiology.en_HK
dc.rightsCopyright © American Society for Microbiology, Journal of virology, 2005, v. 79 n. 10, p. 6180-6193en_HK
dc.subject.meshCommon Cold - geneticsen_HK
dc.subject.meshCoronavirus 229E, Human - genetics - physiologyen_HK
dc.subject.meshCoronavirus Infections - geneticsen_HK
dc.subject.meshSARS Virus - genetics - physiologyen_HK
dc.subject.meshSevere Acute Respiratory Syndrome - geneticsen_HK
dc.titleComparative host gene transcription by microarray analysis early after infection of the Huh7 cell line by severe acute respiratory syndrome coronavirus and human coronavirus 229Een_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-538X&volume=79&issue=10&spage=6180&epage=6193&date=2005&atitle=Comparative+host+gene+transcription+by+microarray+analysis+early+after+infection+of+the+Huh7+cell+line+by+severe+acute+respiratory+syndrome+coronavirus+and+human+coronavirus+229Een_HK
dc.identifier.emailWoo, PCY:pcywoo@hkucc.hku.hken_HK
dc.identifier.emailLau, SKP:skplau@hkucc.hku.hken_HK
dc.identifier.emailChan, TL:tlchan@hku.hken_HK
dc.identifier.emailHung, IFN:ivanhung@hkucc.hku.hken_HK
dc.identifier.emailLeung, SY:suetyi@hkucc.hku.hken_HK
dc.identifier.emailYuen, KY:kyyuen@hkucc.hku.hken_HK
dc.identifier.authorityWoo, PCY=rp00430en_HK
dc.identifier.authorityLau, SKP=rp00486en_HK
dc.identifier.authorityChan, TL=rp00418en_HK
dc.identifier.authorityHung, IFN=rp00508en_HK
dc.identifier.authorityLeung, SY=rp00359en_HK
dc.identifier.authorityYuen, KY=rp00366en_HK
dc.description.naturelink_to_OA_fulltexten_HK
dc.identifier.doi10.1128/JVI.79.10.6180-6193.2005en_HK
dc.identifier.pmid15858003-
dc.identifier.pmcidPMC1091719en_HK
dc.identifier.scopuseid_2-s2.0-20944452287en_HK
dc.identifier.hkuros100322-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-20944452287&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume79en_HK
dc.identifier.issue10en_HK
dc.identifier.spage6180en_HK
dc.identifier.epage6193en_HK
dc.identifier.isiWOS:000228814400030-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTang, BSF=8908243000en_HK
dc.identifier.scopusauthoridChan, KH=7406034307en_HK
dc.identifier.scopusauthoridCheng, VCC=23670479400en_HK
dc.identifier.scopusauthoridWoo, PCY=7201801340en_HK
dc.identifier.scopusauthoridLau, SKP=7401596211en_HK
dc.identifier.scopusauthoridLam, CCK=16947291300en_HK
dc.identifier.scopusauthoridChan, TL=7402687537en_HK
dc.identifier.scopusauthoridWu, AKL=7402998681en_HK
dc.identifier.scopusauthoridHung, IFN=7006103457en_HK
dc.identifier.scopusauthoridLeung, SY=7202044886en_HK
dc.identifier.scopusauthoridYuen, KY=36078079100en_HK

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