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Article: Potent inhibition of SARS-associated coronavirus (SCoV) infection and replication by type I interferons (IFN-α/β) but not by type II interferon (IFN-γ)

TitlePotent inhibition of SARS-associated coronavirus (SCoV) infection and replication by type I interferons (IFN-α/β) but not by type II interferon (IFN-γ)
Authors
Issue Date2004
PublisherMary Ann Liebert, Inc Publishers. The Journal's web site is located at http://www.liebertpub.com/jir
Citation
Journal Of Interferon And Cytokine Research, 2004, v. 24 n. 7, p. 388-390 How to Cite?
AbstractWe sought to investigate the anti-severe acute respiratory syndrome (SARS)-associated coronavirus (SCoV) activities of type I (α and β) and type II (γ) interferons (IFN) in vitro. Type I IFNs protected cells from cytopathic effects (CPE) induced by SCoV, and inhibited viral genomic RNA replication in FRhk-4 cells (measured by quantitative RT-PCR) in a dose-dependent manner. Intracellular viral RNA copies were reduced 50% by IFN-α at a concentration of 25 U/ml and by IFN-β at a concentration of 14 U/ml. IFN-γ had fewer effects on inhibition of viral infection and replication. The type I IFN receptor signaling pathway in host cells is mainly involved in the inhibition of SCoV infection and replication. Type I IFNs could be used as potential agents for anti-SARS treatment.
Persistent Identifierhttp://hdl.handle.net/10722/78960
ISSN
2015 Impact Factor: 2.135
2015 SCImago Journal Rankings: 1.002
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZheng, Ben_HK
dc.contributor.authorHe, MLen_HK
dc.contributor.authorWong, KLen_HK
dc.contributor.authorChing, TLen_HK
dc.contributor.authorPoon, LLMen_HK
dc.contributor.authorPeng, Yen_HK
dc.contributor.authorGuan, Yen_HK
dc.contributor.authorLin, MCMen_HK
dc.contributor.authorKung, HFen_HK
dc.date.accessioned2010-09-06T07:48:53Z-
dc.date.available2010-09-06T07:48:53Z-
dc.date.issued2004en_HK
dc.identifier.citationJournal Of Interferon And Cytokine Research, 2004, v. 24 n. 7, p. 388-390en_HK
dc.identifier.issn1079-9907en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78960-
dc.description.abstractWe sought to investigate the anti-severe acute respiratory syndrome (SARS)-associated coronavirus (SCoV) activities of type I (α and β) and type II (γ) interferons (IFN) in vitro. Type I IFNs protected cells from cytopathic effects (CPE) induced by SCoV, and inhibited viral genomic RNA replication in FRhk-4 cells (measured by quantitative RT-PCR) in a dose-dependent manner. Intracellular viral RNA copies were reduced 50% by IFN-α at a concentration of 25 U/ml and by IFN-β at a concentration of 14 U/ml. IFN-γ had fewer effects on inhibition of viral infection and replication. The type I IFN receptor signaling pathway in host cells is mainly involved in the inhibition of SCoV infection and replication. Type I IFNs could be used as potential agents for anti-SARS treatment.en_HK
dc.languageengen_HK
dc.publisherMary Ann Liebert, Inc Publishers. The Journal's web site is located at http://www.liebertpub.com/jiren_HK
dc.relation.ispartofJournal of Interferon and Cytokine Researchen_HK
dc.rightsThis is a copy of an article published in the Journal of Interferon & Cytokine Research © 2004 [copyright Mary Ann Liebert, Inc.]; Journal of Interferon & Cytokine Research is available online at: http://www.liebertonline.com.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshInterferon Type I - pharmacology-
dc.subject.meshInterferon-gamma - pharmacology-
dc.subject.meshRNA, Viral - biosynthesis-
dc.subject.meshSARS Virus - metabolism - pathogenicity-
dc.subject.meshVirus Replication - drug effects-
dc.titlePotent inhibition of SARS-associated coronavirus (SCoV) infection and replication by type I interferons (IFN-α/β) but not by type II interferon (IFN-γ)en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1079-9907&volume=24&issue=7&spage=388&epage=390&date=2004&atitle=Potent+inhibition+of+SARS-associated+coronavirus+(SCOV)+infection+and+replication+by+type+I+interferons+(IFN-alpha/beta)+but+not+by+type+II+interferon+(IFN-gamma)en_HK
dc.identifier.emailZheng, B: bzheng@hkucc.hku.hken_HK
dc.identifier.emailChing, TL: lumct@hku.hken_HK
dc.identifier.emailPoon, LLM: llmpoon@hkucc.hku.hken_HK
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hken_HK
dc.identifier.emailLin, MCM: mcllin@hkucc.hku.hken_HK
dc.identifier.authorityZheng, B=rp00353en_HK
dc.identifier.authorityChing, TL=rp00757en_HK
dc.identifier.authorityPoon, LLM=rp00484en_HK
dc.identifier.authorityGuan, Y=rp00397en_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1089/1079990041535610en_HK
dc.identifier.pmid15296649-
dc.identifier.scopuseid_2-s2.0-3242885894en_HK
dc.identifier.hkuros91934en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-3242885894&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume24en_HK
dc.identifier.issue7en_HK
dc.identifier.spage388en_HK
dc.identifier.epage390en_HK
dc.identifier.isiWOS:000222991500002-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridZheng, B=7201780588en_HK
dc.identifier.scopusauthoridHe, ML=35080389700en_HK
dc.identifier.scopusauthoridWong, KL=37096563500en_HK
dc.identifier.scopusauthoridChing, TL=7006889374en_HK
dc.identifier.scopusauthoridPoon, LLM=7005441747en_HK
dc.identifier.scopusauthoridPeng, Y=7403419265en_HK
dc.identifier.scopusauthoridGuan, Y=7202924055en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK

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