Significance of the myxovirus resistance A (MxA) gene -123C>a single-nucleotide polymorphism in suppressed interferon beta induction of severe acute respiratory syndrome coronavirus infection.
Identifieur interne : 001591 ( PubMed/Checkpoint ); précédent : 001590; suivant : 001592Significance of the myxovirus resistance A (MxA) gene -123C>a single-nucleotide polymorphism in suppressed interferon beta induction of severe acute respiratory syndrome coronavirus infection.
Auteurs : Johannes Chi-Yun Ching [Hong Kong] ; Kelvin Yuen Kwong Chan ; Eric Hing Leung Lee ; Mei-Shu Xu ; Campbell Kam Po Ting ; Thomas M K. So ; Pak C. Sham ; Gabriel M. Leung ; Joseph S M. Peiris ; Ui-Soon KhooSource :
- The Journal of infectious diseases [ 1537-6613 ] ; 2010.
Descripteurs français
- KwdFr :
- Adolescent, Adulte, Adulte d'âge moyen, Enfant, Enfant d'âge préscolaire, Femelle, Humains, Immunité innée, Interféron alpha (immunologie), Interféron bêta (immunologie), Jeune adulte, Mâle, Polymorphisme de nucléotide simple, Protéines G (génétique), Protéines G (immunologie), Protéines de résistance aux myxovirus, Régions promotrices (génétique), Sujet âgé, Sujet âgé de 80 ans ou plus, Syndrome respiratoire aigu sévère (génétique), Syndrome respiratoire aigu sévère (immunologie), Virus du SRAS (immunologie).
- MESH :
- génétique : Protéines G, Syndrome respiratoire aigu sévère.
- immunologie : Interféron alpha, Interféron bêta, Protéines G, Syndrome respiratoire aigu sévère, Virus du SRAS.
- Adolescent, Adulte, Adulte d'âge moyen, Enfant, Enfant d'âge préscolaire, Femelle, Humains, Immunité innée, Jeune adulte, Mâle, Polymorphisme de nucléotide simple, Protéines de résistance aux myxovirus, Régions promotrices (génétique), Sujet âgé, Sujet âgé de 80 ans ou plus.
English descriptors
- KwdEn :
- Adolescent, Adult, Aged, Aged, 80 and over, Child, Child, Preschool, Female, GTP-Binding Proteins (genetics), GTP-Binding Proteins (immunology), Humans, Immunity, Innate, Interferon-alpha (immunology), Interferon-beta (immunology), Male, Middle Aged, Myxovirus Resistance Proteins, Polymorphism, Single Nucleotide, Promoter Regions, Genetic, SARS Virus (immunology), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (immunology), Young Adult.
- MESH :
- chemical , genetics : GTP-Binding Proteins.
- chemical , immunology : GTP-Binding Proteins, Interferon-alpha, Interferon-beta.
- genetics : Severe Acute Respiratory Syndrome.
- immunology : SARS Virus, Severe Acute Respiratory Syndrome.
- Adolescent, Adult, Aged, Aged, 80 and over, Child, Child, Preschool, Female, Humans, Immunity, Innate, Male, Middle Aged, Myxovirus Resistance Proteins, Polymorphism, Single Nucleotide, Promoter Regions, Genetic, Young Adult.
Abstract
Myxovirus resistance A (MxA) is an antiviral protein induced by interferon alpha and beta (IFN-alpha, IFN-beta) 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-alpha and IFN-beta treatment. Here, we demonstrate that the -123A minor allele provided stronger binding affinity to nuclear proteins extracted from IFN-beta-untreated cells than did the wild-type allele, whereas the -88T allele showed preferential binding after IFN-beta stimulation. Endogenous IFN-alpha and IFN-beta 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 minor-allele 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-alpha and IFN-beta induction such as SARS coronavirus.
DOI: 10.1086/652799
PubMed: 20462354
Affiliations:
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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-alpha and IFN-beta treatment. Here, we demonstrate that the -123A minor allele provided stronger binding affinity to nuclear proteins extracted from IFN-beta-untreated cells than did the wild-type allele, whereas the -88T allele showed preferential binding after IFN-beta stimulation. Endogenous IFN-alpha and IFN-beta 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 minor-allele 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-alpha and IFN-beta induction such as SARS coronavirus.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20462354</PMID><DateCompleted><Year>2010</Year><Month>05</Month><Day>25</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>03</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1537-6613</ISSN><JournalIssue CitedMedium="Internet"><Volume>201</Volume><Issue>12</Issue><PubDate><Year>2010</Year><Month>Jun</Month><Day>15</Day></PubDate></JournalIssue><Title>The Journal of infectious diseases</Title><ISOAbbreviation>J. Infect. Dis.</ISOAbbreviation></Journal><ArticleTitle>Significance of the myxovirus resistance A (MxA) gene -123C>a single-nucleotide polymorphism in suppressed interferon beta induction of severe acute respiratory syndrome coronavirus infection.</ArticleTitle><Pagination><MedlinePgn>1899-908</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1086/652799</ELocationID><Abstract><AbstractText>Myxovirus resistance A (MxA) is an antiviral protein induced by interferon alpha and beta (IFN-alpha, IFN-beta) 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-alpha and IFN-beta treatment. Here, we demonstrate that the -123A minor allele provided stronger binding affinity to nuclear proteins extracted from IFN-beta-untreated cells than did the wild-type allele, whereas the -88T allele showed preferential binding after IFN-beta stimulation. Endogenous IFN-alpha and IFN-beta 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 minor-allele 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-alpha and IFN-beta induction such as SARS coronavirus.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ching</LastName><ForeName>Johannes Chi-Yun</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Hong Kong, Princess Margaret Hospital, Hong Kong.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chan</LastName><ForeName>Kelvin Yuen Kwong</ForeName><Initials>KY</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Eric Hing Leung</ForeName><Initials>EH</Initials></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Mei-Shu</ForeName><Initials>MS</Initials></Author><Author ValidYN="Y"><LastName>Ting</LastName><ForeName>Campbell Kam Po</ForeName><Initials>CK</Initials></Author><Author ValidYN="Y"><LastName>So</LastName><ForeName>Thomas M K</ForeName><Initials>TM</Initials></Author><Author ValidYN="Y"><LastName>Sham</LastName><ForeName>Pak C</ForeName><Initials>PC</Initials></Author><Author ValidYN="Y"><LastName>Leung</LastName><ForeName>Gabriel M</ForeName><Initials>GM</Initials></Author><Author ValidYN="Y"><LastName>Peiris</LastName><ForeName>Joseph S M</ForeName><Initials>JS</Initials></Author><Author ValidYN="Y"><LastName>Khoo</LastName><ForeName>Ui-Soon</ForeName><Initials>US</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Infect Dis</MedlineTA><NlmUniqueID>0413675</NlmUniqueID><ISSNLinking>0022-1899</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016898">Interferon-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C579071">MX1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D064547">Myxovirus Resistance Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>77238-31-4</RegistryNumber><NameOfSubstance UI="D016899">Interferon-beta</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.6.1.-</RegistryNumber><NameOfSubstance UI="D019204">GTP-Binding Proteins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002675" MajorTopicYN="N">Child, Preschool</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019204" MajorTopicYN="N">GTP-Binding Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007113" MajorTopicYN="N">Immunity, Innate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016898" MajorTopicYN="N">Interferon-alpha</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016899" MajorTopicYN="N">Interferon-beta</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D064547" MajorTopicYN="N">Myxovirus Resistance Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020641" MajorTopicYN="Y">Polymorphism, Single Nucleotide</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011401" MajorTopicYN="Y">Promoter Regions, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045473" 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Leung</name><name sortKey="Peiris, Joseph S M" sort="Peiris, Joseph S M" uniqKey="Peiris J" first="Joseph S M" last="Peiris">Joseph S M. Peiris</name><name sortKey="Sham, Pak C" sort="Sham, Pak C" uniqKey="Sham P" first="Pak C" last="Sham">Pak C. Sham</name><name sortKey="So, Thomas M K" sort="So, Thomas M K" uniqKey="So T" first="Thomas M K" last="So">Thomas M K. So</name><name sortKey="Ting, Campbell Kam Po" sort="Ting, Campbell Kam Po" uniqKey="Ting C" first="Campbell Kam Po" last="Ting">Campbell Kam Po Ting</name><name sortKey="Xu, Mei Shu" sort="Xu, Mei Shu" uniqKey="Xu M" first="Mei-Shu" last="Xu">Mei-Shu Xu</name></noCountry><country name="Hong Kong"><noRegion><name sortKey="Ching, Johannes Chi Yun" sort="Ching, Johannes Chi Yun" uniqKey="Ching J" first="Johannes Chi-Yun" last="Ching">Johannes Chi-Yun Ching</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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