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Statements

Subject Item
n2:RIV%2F00216208%3A11130%2F11%3A7140%21RIV12-MZ0-11130___
rdf:type
skos:Concept n14:Vysledek
rdfs:seeAlso
http://www.ncbi.nlm.nih.gov/pubmed/22110759
dcterms:description
Interferon induced with helicase C domain 1 (IFIH1) senses and initiates antiviral activity against enteroviruses. Genetic variants of IFIH1, one common and four rare SNPs have been associated with lower risk for type 1 diabetes. Our aim was to test whether these type 1 diabetes-associated IFIH1 polymorphisms are associated with the occurrence of enterovirus infection in the gut of healthy children, or influence the lack of association between gut enterovirus infection and islet autoimmunity. After testing of 46,939 Norwegian newborns, 421 children carrying the high risk genotype for type 1 diabetes (HLA-DR4-DQ8/DR3-DQ2) as well as 375 children without this genotype were included for monthly fecal collections from 3 to 35 months of age, and genotyped for the IFIH1 polymorphisms. A total of 7,793 fecal samples were tested for presence of enterovirus RNA using real time reverse transcriptase PCR. We found no association with frequency of enterovirus in the gut for the common IFIH1 polymorphism rs1990760, or either of the rare variants of rs35744605, rs35667974, rs35337543, while the enterovirus prevalence marginally differed in samples from the 8 carriers of a rare allele of rs35732034 (26.1%, 18/69 samples) as compared to wild-type homozygotes (12.4%, 955/7724 samples); odds ratio 2.5, p = 0.06. The association was stronger when infections were restricted to those with high viral loads (odds ratio 3.3, 95% CI 1.3-8.4, p = 0.01). The lack of association between enterovirus frequency and islet autoimmunity reported in our previous study was not materially influenced by the IFIH1 SNPs. We conclude that the type 1 diabetes-associated IFIH1 polymorphisms have no, or only minor influence on the occurrence, quantity or duration of enterovirus infection in the gut. Its effect on the risk of diabetes is likely to lie elsewhere in the pathogenic process than in the modification of gut infection. Interferon induced with helicase C domain 1 (IFIH1) senses and initiates antiviral activity against enteroviruses. Genetic variants of IFIH1, one common and four rare SNPs have been associated with lower risk for type 1 diabetes. Our aim was to test whether these type 1 diabetes-associated IFIH1 polymorphisms are associated with the occurrence of enterovirus infection in the gut of healthy children, or influence the lack of association between gut enterovirus infection and islet autoimmunity. After testing of 46,939 Norwegian newborns, 421 children carrying the high risk genotype for type 1 diabetes (HLA-DR4-DQ8/DR3-DQ2) as well as 375 children without this genotype were included for monthly fecal collections from 3 to 35 months of age, and genotyped for the IFIH1 polymorphisms. A total of 7,793 fecal samples were tested for presence of enterovirus RNA using real time reverse transcriptase PCR. We found no association with frequency of enterovirus in the gut for the common IFIH1 polymorphism rs1990760, or either of the rare variants of rs35744605, rs35667974, rs35337543, while the enterovirus prevalence marginally differed in samples from the 8 carriers of a rare allele of rs35732034 (26.1%, 18/69 samples) as compared to wild-type homozygotes (12.4%, 955/7724 samples); odds ratio 2.5, p = 0.06. The association was stronger when infections were restricted to those with high viral loads (odds ratio 3.3, 95% CI 1.3-8.4, p = 0.01). The lack of association between enterovirus frequency and islet autoimmunity reported in our previous study was not materially influenced by the IFIH1 SNPs. We conclude that the type 1 diabetes-associated IFIH1 polymorphisms have no, or only minor influence on the occurrence, quantity or duration of enterovirus infection in the gut. Its effect on the risk of diabetes is likely to lie elsewhere in the pathogenic process than in the modification of gut infection.
dcterms:title
Polymorphisms in the Innate Immune IFIH1 Gene, Frequency of Enterovirus in Monthly Fecal Samples during Infancy, and Islet Autoimmunity Polymorphisms in the Innate Immune IFIH1 Gene, Frequency of Enterovirus in Monthly Fecal Samples during Infancy, and Islet Autoimmunity
skos:prefLabel
Polymorphisms in the Innate Immune IFIH1 Gene, Frequency of Enterovirus in Monthly Fecal Samples during Infancy, and Islet Autoimmunity Polymorphisms in the Innate Immune IFIH1 Gene, Frequency of Enterovirus in Monthly Fecal Samples during Infancy, and Islet Autoimmunity
skos:notation
RIV/00216208:11130/11:7140!RIV12-MZ0-11130___
n14:predkladatel
n15:orjk%3A11130
n3:aktivita
n6:P n6:I
n3:aktivity
I, P(NT11465)
n3:cisloPeriodika
11
n3:dodaniDat
n12:2012
n3:domaciTvurceVysledku
n11:7384874
n3:druhVysledku
n19:J
n3:duvernostUdaju
n17:S
n3:entitaPredkladatele
n16:predkladatel
n3:idSjednocenehoVysledku
221258
n3:idVysledku
RIV/00216208:11130/11:7140
n3:jazykVysledku
n9:eng
n3:klicovaSlova
beta-cell autoimmunity; blood mononuclear-cells; function mutations; risk-factor; rig-i; type-1; infections; rna; association; children
n3:klicoveSlovo
n5:function%20mutations n5:rna n5:infections n5:beta-cell%20autoimmunity n5:risk-factor n5:association n5:type-1 n5:blood%20mononuclear-cells n5:rig-i n5:children
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[090E679B6B5F]
n3:nazevZdroje
PLoS One
n3:obor
n4:FP
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
6
n3:projekt
n20:NT11465
n3:rokUplatneniVysledku
n12:2011
n3:svazekPeriodika
6
n3:tvurceVysledku
Witso, E. Ronningen, KS Pociot, FM Tapia, G. Cinek, Ondřej Stene, LC
n3:wos
000297554300053
s:issn
1932-6203
s:numberOfPages
6
n10:organizacniJednotka
11130