Significance of the Myxovirus Resistance A (MxA) Gene — 123C>A Single-Nucleotide Polymorphism in Suppressed Interferon β Induction of Severe Acute Respiratory Syndrome Coronavirus Infection
Identifieur interne : 000097 ( Psycho/Analysis ); précédent : 000096; suivant : 000098Significance of the Myxovirus Resistance A (MxA) Gene — 123C>A Single-Nucleotide Polymorphism in Suppressed Interferon β Induction of Severe Acute Respiratory Syndrome Coronavirus Infection
Auteurs : Johannes Chi-Yun Ching [Hong Kong] ; Kelvin Yuen Kwong Chan [Hong Kong] ; Eric Hing Leung Lee [Hong Kong] ; Mei-Shu Xu [Hong Kong] ; Campbell Kam Po Ting [Hong Kong] ; Thomas M. K. So [Hong Kong] ; Pak C. Sham [Hong Kong] ; Gabriel M. Leung [Hong Kong] ; Joseph S. M. Peiris [Hong Kong] ; Ui-Soon Khoo [Hong Kong]Source :
- The Journal of Infectious Diseases [ 0022-1899 ] ; 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.
- Pascal (Inist)
English descriptors
- KwdEn :
- Adolescent, Adult, Aged, Aged, 80 and over, Beta interferon, Child, Child, Preschool, Coronavirus, Female, GTP-Binding Proteins (genetics), GTP-Binding Proteins (immunology), Gene, Humans, Immunity, Innate, Infection, Interferon-alpha (immunology), Interferon-beta (immunology), Male, Middle Aged, Myxovirus Resistance Proteins, Polymorphism, Single Nucleotide, Promoter Regions, Genetic, Resistance, SARS Virus (immunology), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (immunology), Severe acute respiratory syndrome, Single nucleotide polymorphism, 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 α and β (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.
Url:
- https://api.istex.fr/ark:/67375/HXZ-FD1L73MB-Q/fulltext.pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7109798
DOI: 10.1086/652799
Affiliations:
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type="main">Significance of the Myxovirus Resistance A (MxA) Gene — 123C>A Single-Nucleotide Polymorphism in Suppressed Interferon β Induction of Severe Acute Respiratory Syndrome Coronavirus Infection</title><author><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><affiliation wicri:level="1"><country xml:lang="fr">Hong Kong</country><wicri:regionArea>Department of Pathology, University of Hong Kong</wicri:regionArea><wicri:noRegion>University of Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Chan, Kelvin Yuen Kwong" sort="Chan, Kelvin Yuen Kwong" uniqKey="Chan K" first="Kelvin Yuen Kwong" last="Chan">Kelvin Yuen Kwong Chan</name><affiliation wicri:level="1"><country xml:lang="fr">Hong Kong</country><wicri:regionArea>Department of Pathology, University of Hong Kong</wicri:regionArea><wicri:noRegion>University of Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Lee, Eric Hing Leung" sort="Lee, Eric Hing Leung" uniqKey="Lee E" first="Eric Hing Leung" last="Lee">Eric Hing Leung Lee</name><affiliation wicri:level="1"><country xml:lang="fr">Hong Kong</country><wicri:regionArea>Department of Pathology, University of Hong Kong</wicri:regionArea><wicri:noRegion>University of Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Xu, Mei Shu" sort="Xu, Mei Shu" uniqKey="Xu M" first="Mei-Shu" last="Xu">Mei-Shu Xu</name><affiliation wicri:level="1"><country xml:lang="fr">Hong Kong</country><wicri:regionArea>Department of Pathology, University of Hong Kong</wicri:regionArea><wicri:noRegion>University of Hong Kong</wicri:noRegion></affiliation></author><author><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><affiliation wicri:level="1"><country xml:lang="fr">Hong 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type="eISSN">1537-6613</idno><imprint><publisher>The University of Chicago Press</publisher><date type="published">2010</date><biblScope unit="vol">201</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="1899">1899</biblScope><biblScope unit="page" to="1908">1908</biblScope></imprint><idno type="ISSN">0022-1899</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-1899</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Beta interferon</term><term>Child</term><term>Child, Preschool</term><term>Coronavirus</term><term>Female</term><term>GTP-Binding Proteins (genetics)</term><term>GTP-Binding Proteins (immunology)</term><term>Gene</term><term>Humans</term><term>Immunity, Innate</term><term>Infection</term><term>Interferon-alpha (immunology)</term><term>Interferon-beta (immunology)</term><term>Male</term><term>Middle Aged</term><term>Myxovirus Resistance Proteins</term><term>Polymorphism, Single Nucleotide</term><term>Promoter Regions, Genetic</term><term>Resistance</term><term>SARS Virus (immunology)</term><term>Severe Acute Respiratory Syndrome (genetics)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe acute respiratory syndrome</term><term>Single nucleotide polymorphism</term><term>Young Adult</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adolescent</term><term>Adulte</term><term>Adulte d'âge moyen</term><term>Enfant</term><term>Enfant d'âge préscolaire</term><term>Femelle</term><term>Humains</term><term>Immunité innée</term><term>Interféron alpha (immunologie)</term><term>Interféron bêta (immunologie)</term><term>Jeune adulte</term><term>Mâle</term><term>Polymorphisme de nucléotide simple</term><term>Protéines G (génétique)</term><term>Protéines G (immunologie)</term><term>Protéines de résistance aux myxovirus</term><term>Régions promotrices (génétique)</term><term>Sujet âgé</term><term>Sujet âgé de 80 ans ou plus</term><term>Syndrome respiratoire aigu sévère (génétique)</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>GTP-Binding Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>GTP-Binding Proteins</term><term>Interferon-alpha</term><term>Interferon-beta</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines G</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Interféron alpha</term><term>Interféron bêta</term><term>Protéines G</term><term>Syndrome respiratoire aigu sévère</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Child</term><term>Child, Preschool</term><term>Female</term><term>Humans</term><term>Immunity, Innate</term><term>Male</term><term>Middle Aged</term><term>Myxovirus Resistance Proteins</term><term>Polymorphism, Single Nucleotide</term><term>Promoter Regions, Genetic</term><term>Young Adult</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adolescent</term><term>Adulte</term><term>Adulte d'âge moyen</term><term>Enfant</term><term>Enfant d'âge préscolaire</term><term>Femelle</term><term>Humains</term><term>Immunité innée</term><term>Jeune adulte</term><term>Mâle</term><term>Polymorphisme de nucléotide simple</term><term>Protéines de résistance aux myxovirus</term><term>Régions promotrices (génétique)</term><term>Sujet âgé</term><term>Sujet âgé de 80 ans ou plus</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Coronavirus</term><term>Gène</term><term>Infection</term><term>Interféron bêta</term><term>Polymorphisme mononucléotide</term><term>Résistance</term><term>Syndrome respiratoire aigu sévère</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract">Myxovirus resistance A (MxA) is an antiviral protein induced by interferon α and β (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.</div></front></TEI><affiliations><list><country><li>Hong Kong</li></country></list><tree><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><name sortKey="Chan, Kelvin Yuen Kwong" sort="Chan, Kelvin Yuen Kwong" uniqKey="Chan K" first="Kelvin Yuen Kwong" last="Chan">Kelvin Yuen Kwong Chan</name><name sortKey="Khoo, Ui Soon" sort="Khoo, Ui Soon" uniqKey="Khoo U" first="Ui-Soon" last="Khoo">Ui-Soon Khoo</name><name sortKey="Khoo, Ui Soon" sort="Khoo, Ui Soon" uniqKey="Khoo U" first="Ui-Soon" last="Khoo">Ui-Soon Khoo</name><name sortKey="Lee, Eric Hing Leung" sort="Lee, Eric Hing Leung" uniqKey="Lee E" first="Eric Hing Leung" last="Lee">Eric Hing Leung Lee</name><name sortKey="Leung, Gabriel M" sort="Leung, Gabriel M" uniqKey="Leung G" first="Gabriel M." last="Leung">Gabriel M. 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></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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