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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
Funding AgencyGrant Number
Control of Infectious Diseases, Hong Kong SAR Government04050252
University of Hong Kong200511159125
Funding Information:

We thank Dr Vivian Wong and Ms Edwina Shung (Hospital Authority Severe Acute Respiratory Syndrome Collaborative Group) for the retrieval of clinical data of SARS patients from the central database. This work was supported by the Research Fund for the Control of Infectious Diseases, Hong Kong SAR Government (Project 04050252) and Seed Funding Programme for Basic Research, The University of Hong Kong (Project 200511159125).

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-

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