File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Significance of the Myxovirus resistance A (MxA) gene - 123C>A single-nucleotide polymorphism in suppressed interferon ß induction of severe acute respiratory syndrome coronavirus infection

TitleSignificance of the Myxovirus resistance A (MxA) gene - 123C>A single-nucleotide polymorphism in suppressed interferon ß induction of severe acute respiratory syndrome coronavirus infection
Authors
Issue Date2010
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
Citation
Journal Of Infectious Diseases, 2010, v. 201 n. 12, p. 1899-1908 How to Cite?
AbstractMyxovirus resistance A (MxA) is an antiviral protein induced by interferon a and ß (IFN-α, IFN-β) that can inhibit viral replication. The minor alleles of the -88G>T and -123C>A MxA promoter single-nucleotide polymorphisms (SNPs) are associated with increased promoter activity and altered response to IFN-α and IFN-β treatment. Here, we demonstrate that the -123A minor allele provided stronger binding affinity to nuclear proteins extracted from IFN-β-untreated cells than did the wild-type allele, whereas the -88T allele showed preferential binding after IFN-β stimulation. Endogenous IFN-α and IFN-β induction can be suppressed in severe acute respiratory syndrome (SARS) Coronavirus infection. In support of our in vitro findings, a large case-control genetic-association study for SARS Coronavirus infection confirmed that the -123A minor-allele carriers were significantly associated with lower risk of SARS Coronavirus infection, whereas the -88T minorallele carriers were insignificant after adjustment for confounding effects. This suggests that -123C>A plays a more important role in modulating basal MxA expression, thus contributing more significantly to innate immune response against viral infections that suppress endogenous IFN-α and IFN-β induction such as SARS Coronavirus. © 2010 by the Infectious Diseases Society of America. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/148620
ISSN
2015 Impact Factor: 6.344
2015 SCImago Journal Rankings: 4.000
ISI Accession Number ID
References
Grants

 

DC FieldValueLanguage
dc.contributor.authorChing, JCYen_HK
dc.contributor.authorChan, KYKen_HK
dc.contributor.authorLee, EHLen_HK
dc.contributor.authorXu, MSen_HK
dc.contributor.authorTing, CKPen_HK
dc.contributor.authorSo, TMKen_HK
dc.contributor.authorSham, PCen_HK
dc.contributor.authorLeung, GMen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.contributor.authorKhoo, USen_HK
dc.date.accessioned2012-05-29T06:14:09Z-
dc.date.available2012-05-29T06:14:09Z-
dc.date.issued2010en_HK
dc.identifier.citationJournal Of Infectious Diseases, 2010, v. 201 n. 12, p. 1899-1908en_HK
dc.identifier.issn0022-1899en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148620-
dc.description.abstractMyxovirus resistance A (MxA) is an antiviral protein induced by interferon a and ß (IFN-α, IFN-β) that can inhibit viral replication. The minor alleles of the -88G>T and -123C>A MxA promoter single-nucleotide polymorphisms (SNPs) are associated with increased promoter activity and altered response to IFN-α and IFN-β treatment. Here, we demonstrate that the -123A minor allele provided stronger binding affinity to nuclear proteins extracted from IFN-β-untreated cells than did the wild-type allele, whereas the -88T allele showed preferential binding after IFN-β stimulation. Endogenous IFN-α and IFN-β induction can be suppressed in severe acute respiratory syndrome (SARS) Coronavirus infection. In support of our in vitro findings, a large case-control genetic-association study for SARS Coronavirus infection confirmed that the -123A minor-allele carriers were significantly associated with lower risk of SARS Coronavirus infection, whereas the -88T minorallele carriers were insignificant after adjustment for confounding effects. This suggests that -123C>A plays a more important role in modulating basal MxA expression, thus contributing more significantly to innate immune response against viral infections that suppress endogenous IFN-α and IFN-β induction such as SARS Coronavirus. © 2010 by the Infectious Diseases Society of America. All rights reserved.en_HK
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.orgen_HK
dc.relation.ispartofJournal of Infectious Diseasesen_HK
dc.subject.meshAdolescenten_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshAged, 80 And Overen_US
dc.subject.meshChilden_US
dc.subject.meshChild, Preschoolen_US
dc.subject.meshFemaleen_US
dc.subject.meshGtp-Binding Proteins - Genetics - Immunologyen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunity, Innateen_US
dc.subject.meshInterferon-Alpha - Immunologyen_US
dc.subject.meshInterferon-Beta - Immunologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPolymorphism, Single Nucleotideen_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshSars Virus - Immunologyen_US
dc.subject.meshSevere Acute Respiratory Syndrome - Genetics - Immunologyen_US
dc.subject.meshYoung Adulten_US
dc.titleSignificance of the Myxovirus resistance A (MxA) gene - 123C>A single-nucleotide polymorphism in suppressed interferon ß induction of severe acute respiratory syndrome coronavirus infectionen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, KYK: kelvinc@pathology.hku.hken_HK
dc.identifier.emailSham, PC: pcsham@hku.hken_HK
dc.identifier.emailLeung, GM: gmleung@hku.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.emailKhoo, US: uskhoo@hku.hken_HK
dc.identifier.authorityChan, KYK=rp00453en_HK
dc.identifier.authoritySham, PC=rp00459en_HK
dc.identifier.authorityLeung, GM=rp00460en_HK
dc.identifier.authorityPeiris, JSM=rp00410en_HK
dc.identifier.authorityKhoo, US=rp00362en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1086/652799en_HK
dc.identifier.pmid20462354-
dc.identifier.scopuseid_2-s2.0-77952560927en_HK
dc.identifier.hkuros174295-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77952560927&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume201en_HK
dc.identifier.issue12en_HK
dc.identifier.spage1899en_HK
dc.identifier.epage1908en_HK
dc.identifier.eissn1537-6613-
dc.identifier.isiWOS:000277687900016-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectPromoter polymorphisms of DC-SIGN in relation to host genetic susceptibility to SARS infection-
dc.identifier.scopusauthoridChing, JCY=15735635300en_HK
dc.identifier.scopusauthoridChan, KYK=7406034195en_HK
dc.identifier.scopusauthoridLee, EHL=36061087000en_HK
dc.identifier.scopusauthoridXu, MS=35957113100en_HK
dc.identifier.scopusauthoridTing, CKP=36061321600en_HK
dc.identifier.scopusauthoridSo, TMK=7005305634en_HK
dc.identifier.scopusauthoridSham, PC=34573429300en_HK
dc.identifier.scopusauthoridLeung, GM=7007159841en_HK
dc.identifier.scopusauthoridPeiris, JSM=7005486823en_HK
dc.identifier.scopusauthoridKhoo, US=7004195799en_HK
dc.identifier.citeulike7182114-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats