SrasV1, PascalFrancis, Corpus, bibRecord, 000152

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 : 000152 ( PascalFrancis/Corpus ); précédent : 000151; suivant : 000153

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

Auteurs : Johannes Chi-Yun Ching ; 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 Khoo

Source :

The Journal of infectious diseases [ 0022-1899 ] ; 2010.

RBID : Pascal:10-0302334

Descripteurs français

Pascal (Inist)
- Coronavirus, Résistance, Gène, Polymorphisme mononucléotide, Infection, Interféron bêta, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Beta interferon, Coronavirus, Gene, Infection, Resistance, Severe acute respiratory syndrome, Single nucleotide polymorphism.

Abstract

Myxovirus resistance A (MxA) is an antiviral protein induced by interferon α and β (IFN-α, If-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 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-α and IFN-β induction such as SARS coronavirus.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A02	`01`			`@0 JIDIAQ`
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A05				`@2 201`
A06				`@2 12`
A08	`01`	`1`	`ENG`	`@1 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`
A11	`01`	`1`		`@1 CHING (Johannes Chi-Yun)`
A11	`02`	`1`		`@1 YUEN KWONG CHAN (Kelvin)`
A11	`03`	`1`		`@1 HING LEUNG LEE (Eric)`
A11	`04`	`1`		`@1 XU (Mei-Shu)`
A11	`05`	`1`		`@1 KAM PO TING (Campbell)`
A11	`06`	`1`		`@1 SO (Thomas M. K.)`
A11	`07`	`1`		`@1 SHAM (Pak C.)`
A11	`08`	`1`		`@1 LEUNG (Gabriel M.)`
A11	`09`	`1`		`@1 PEIRIS (Joseph S. M.)`
A11	`10`	`1`		`@1 KHOO (Ui-Soon)`
A14	`01`			`@1 Department of Pathology, University of Hong Kong @3 HKG @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 10 aut.`
A14	`02`			`@1 Department of Psychiatry, University of Hong Kong @3 HKG @Z 7 aut.`
A14	`03`			`@1 Department of Community Medicine, University of Hong Kong @3 HKG @Z 8 aut.`
A14	`04`			`@1 Department of Microbiology, University of Hong Kong @3 HKG @Z 9 aut.`
A14	`05`			`@1 Department of Medicine and Geriatrics, Princess Margaret Hospital @3 HKG @Z 6 aut.`
A20				`@1 1899-1908`
A21				`@1 2010`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 2052 @5 354000193044770160`
A44				`@0 0000 @1 © 2010 INIST-CNRS. All rights reserved.`
A45				`@0 42 ref.`
A47	`01`	`1`		`@0 10-0302334`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 The Journal of infectious diseases`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 Myxovirus resistance A (MxA) is an antiviral protein induced by interferon α and β (IFN-α, If-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 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-α and IFN-β induction such as SARS coronavirus.
C02	`01`	`X`		`@0 002A05C10`
C02	`02`	`X`		`@0 002B05`
C03	`01`	`X`	`FRE`	`@0 Coronavirus @2 NW @5 01`
C03	`01`	`X`	`ENG`	`@0 Coronavirus @2 NW @5 01`
C03	`01`	`X`	`SPA`	`@0 Coronavirus @2 NW @5 01`
C03	`02`	`X`	`FRE`	`@0 Résistance @5 05`
C03	`02`	`X`	`ENG`	`@0 Resistance @5 05`
C03	`02`	`X`	`SPA`	`@0 Resistencia @5 05`
C03	`03`	`X`	`FRE`	`@0 Gène @5 06`
C03	`03`	`X`	`ENG`	`@0 Gene @5 06`
C03	`03`	`X`	`SPA`	`@0 Gen @5 06`
C03	`04`	`X`	`FRE`	`@0 Polymorphisme mononucléotide @5 07`
C03	`04`	`X`	`ENG`	`@0 Single nucleotide polymorphism @5 07`
C03	`04`	`X`	`SPA`	`@0 Polimorfismo mononucleótido @5 07`
C03	`05`	`X`	`FRE`	`@0 Infection @5 08`
C03	`05`	`X`	`ENG`	`@0 Infection @5 08`
C03	`05`	`X`	`SPA`	`@0 Infección @5 08`
C03	`06`	`X`	`FRE`	`@0 Interféron bêta @2 FR @5 14`
C03	`06`	`X`	`ENG`	`@0 Beta interferon @2 FR @5 14`
C03	`06`	`X`	`SPA`	`@0 Interferón beta @2 FR @5 14`
C03	`07`	`X`	`FRE`	`@0 Syndrome respiratoire aigu sévère @2 NM @5 15`
C03	`07`	`X`	`ENG`	`@0 Severe acute respiratory syndrome @2 NM @5 15`
C03	`07`	`X`	`SPA`	`@0 Síndrome respiratorio agudo severo @2 NM @5 15`
C07	`01`	`X`	`FRE`	`@0 Coronaviridae @2 NW`
C07	`01`	`X`	`ENG`	`@0 Coronaviridae @2 NW`
C07	`01`	`X`	`SPA`	`@0 Coronaviridae @2 NW`
C07	`02`	`X`	`FRE`	`@0 Nidovirales @2 NW`
C07	`02`	`X`	`ENG`	`@0 Nidovirales @2 NW`
C07	`02`	`X`	`SPA`	`@0 Nidovirales @2 NW`
C07	`03`	`X`	`FRE`	`@0 Virus @2 NW`
C07	`03`	`X`	`ENG`	`@0 Virus @2 NW`
C07	`03`	`X`	`SPA`	`@0 Virus @2 NW`
C07	`04`	`X`	`FRE`	`@0 Cytokine @5 13`
C07	`04`	`X`	`ENG`	`@0 Cytokine @5 13`
C07	`04`	`X`	`SPA`	`@0 Citoquina @5 13`
C07	`05`	`X`	`FRE`	`@0 Virose`
C07	`05`	`X`	`ENG`	`@0 Viral disease`
C07	`05`	`X`	`SPA`	`@0 Virosis`
C07	`06`	`X`	`FRE`	`@0 Pathologie de l'appareil respiratoire @5 16`
C07	`06`	`X`	`ENG`	`@0 Respiratory disease @5 16`
C07	`06`	`X`	`SPA`	`@0 Aparato respiratorio patología @5 16`
C07	`07`	`X`	`FRE`	`@0 Pathologie des poumons @5 17`
C07	`07`	`X`	`ENG`	`@0 Lung disease @5 17`
C07	`07`	`X`	`SPA`	`@0 Pulmón patología @5 17`
N21				`@1 193`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 10-0302334 INIST
ET :	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
AU :	CHING (Johannes Chi-Yun); YUEN KWONG CHAN (Kelvin); HING LEUNG LEE (Eric); XU (Mei-Shu); KAM PO TING (Campbell); SO (Thomas M. K.); SHAM (Pak C.); LEUNG (Gabriel M.); PEIRIS (Joseph S. M.); KHOO (Ui-Soon)
AF :	Department of Pathology, University of Hong Kong/Hong-Kong (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 10 aut.); Department of Psychiatry, University of Hong Kong/Hong-Kong (7 aut.); Department of Community Medicine, University of Hong Kong/Hong-Kong (8 aut.); Department of Microbiology, University of Hong Kong/Hong-Kong (9 aut.); Department of Medicine and Geriatrics, Princess Margaret Hospital/Hong-Kong (6 aut.)
DT :	Publication en série; Niveau analytique
SO :	The Journal of infectious diseases; ISSN 0022-1899; Coden JIDIAQ; Etats-Unis; Da. 2010; Vol. 201; No. 12; Pp. 1899-1908; Bibl. 42 ref.
LA :	Anglais
EA :	Myxovirus resistance A (MxA) is an antiviral protein induced by interferon α and β (IFN-α, If-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 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-α and IFN-β induction such as SARS coronavirus.
CC :	002A05C10; 002B05
FD :	Coronavirus; Résistance; Gène; Polymorphisme mononucléotide; Infection; Interféron bêta; Syndrome respiratoire aigu sévère
FG :	Coronaviridae; Nidovirales; Virus; Cytokine; Virose; Pathologie de l'appareil respiratoire; Pathologie des poumons
ED :	Coronavirus; Resistance; Gene; Single nucleotide polymorphism; Infection; Beta interferon; Severe acute respiratory syndrome
EG :	Coronaviridae; Nidovirales; Virus; Cytokine; Viral disease; Respiratory disease; Lung disease
SD :	Coronavirus; Resistencia; Gen; Polimorfismo mononucleótido; Infección; Interferón beta; Síndrome respiratorio agudo severo
LO :	INIST-2052.354000193044770160
ID :	10-0302334

Links to Exploration step

Pascal:10-0302334

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">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>
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<front><div type="abstract" xml:lang="en">Myxovirus resistance A (MxA) is an antiviral protein induced by interferon α and β (IFN-α, If-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 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-α and IFN-β induction such as SARS coronavirus.</div>
</front>
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<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-1899</s0>
</fA01>
<fA02 i1="01"><s0>JIDIAQ</s0>
</fA02>
<fA03 i2="1"><s0>J. infect. dis.</s0>
</fA03>
<fA05><s2>201</s2>
</fA05>
<fA06><s2>12</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>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</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>CHING (Johannes Chi-Yun)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>YUEN KWONG CHAN (Kelvin)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>HING LEUNG LEE (Eric)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>XU (Mei-Shu)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>KAM PO TING (Campbell)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>SO (Thomas M. K.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>SHAM (Pak C.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>LEUNG (Gabriel M.)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>PEIRIS (Joseph S. M.)</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>KHOO (Ui-Soon)</s1>
</fA11>
<fA14 i1="01"><s1>Department of Pathology, University of Hong Kong</s1>
<s3>HKG</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Psychiatry, University of Hong Kong</s1>
<s3>HKG</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Community Medicine, University of Hong Kong</s1>
<s3>HKG</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Microbiology, University of Hong Kong</s1>
<s3>HKG</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Medicine and Geriatrics, Princess Margaret Hospital</s1>
<s3>HKG</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA20><s1>1899-1908</s1>
</fA20>
<fA21><s1>2010</s1>
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<fA23 i1="01"><s0>ENG</s0>
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<s1>© 2010 INIST-CNRS. All rights reserved.</s1>
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<fA45><s0>42 ref.</s0>
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<fA47 i1="01" i2="1"><s0>10-0302334</s0>
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<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>The Journal of infectious diseases</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Myxovirus resistance A (MxA) is an antiviral protein induced by interferon α and β (IFN-α, If-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 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-α and IFN-β induction such as SARS coronavirus.</s0>
</fC01>
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<server><NO>PASCAL 10-0302334 INIST</NO>
<ET>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</ET>
<AU>CHING (Johannes Chi-Yun); YUEN KWONG CHAN (Kelvin); HING LEUNG LEE (Eric); XU (Mei-Shu); KAM PO TING (Campbell); SO (Thomas M. K.); SHAM (Pak C.); LEUNG (Gabriel M.); PEIRIS (Joseph S. M.); KHOO (Ui-Soon)</AU>
<AF>Department of Pathology, University of Hong Kong/Hong-Kong (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 10 aut.); Department of Psychiatry, University of Hong Kong/Hong-Kong (7 aut.); Department of Community Medicine, University of Hong Kong/Hong-Kong (8 aut.); Department of Microbiology, University of Hong Kong/Hong-Kong (9 aut.); Department of Medicine and Geriatrics, Princess Margaret Hospital/Hong-Kong (6 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>The Journal of infectious diseases; ISSN 0022-1899; Coden JIDIAQ; Etats-Unis; Da. 2010; Vol. 201; No. 12; Pp. 1899-1908; Bibl. 42 ref.</SO>
<LA>Anglais</LA>
<EA>Myxovirus resistance A (MxA) is an antiviral protein induced by interferon α and β (IFN-α, If-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 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-α and IFN-β induction such as SARS coronavirus.</EA>
<CC>002A05C10; 002B05</CC>
<FD>Coronavirus; Résistance; Gène; Polymorphisme mononucléotide; Infection; Interféron bêta; Syndrome respiratoire aigu sévère</FD>
<FG>Coronaviridae; Nidovirales; Virus; Cytokine; Virose; Pathologie de l'appareil respiratoire; Pathologie des poumons</FG>
<ED>Coronavirus; Resistance; Gene; Single nucleotide polymorphism; Infection; Beta interferon; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Cytokine; Viral disease; Respiratory disease; Lung disease</EG>
<SD>Coronavirus; Resistencia; Gen; Polimorfismo mononucleótido; Infección; Interferón beta; Síndrome respiratorio agudo severo</SD>
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<ID>10-0302334</ID>
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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

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

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