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Parechovirus Infection in Early Childhood and Association With Subsequent Celiac Disease
G. Tapia, K. Chudá, CR. Kahrs, LC. Stene, L. Kramna, K. Mårild, T. Rasmussen, KS. Rønningen, O. Cinek, K. Størdal
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
ProQuest Central
from 2020-01-01 to 1 year ago
Health & Medicine (ProQuest)
from 2020-01-01 to 1 year ago
- MeSH
- Autoimmunity * MeSH
- Autoantibodies blood MeSH
- Celiac Disease diagnosis immunology virology MeSH
- Child MeSH
- Infant MeSH
- Humans MeSH
- Follow-Up Studies MeSH
- Parechovirus immunology MeSH
- Picornaviridae Infections diagnosis immunology virology MeSH
- Child, Preschool MeSH
- Antibodies, Viral immunology MeSH
- Risk Factors MeSH
- Case-Control Studies MeSH
- Age Factors MeSH
- Check Tag
- Child MeSH
- Infant MeSH
- Humans MeSH
- Male MeSH
- Child, Preschool MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
INTRODUCTION: To test whether parechovirus and anellovirus, frequent enteric viruses, were associated with subsequent celiac disease (CD). We hypothesized that children who later developed CD would have increased frequency of parechovirus infections before transglutaminase 2 (TG2) antibody development. Anellovirus testing was exploratory, as a potential marker of immune status. METHODS: Matched case-control design nested within a longitudinal birth cohort (the MIDIA study) of children at genetic risk of CD (carrying the human leukocyte antigen genotype DR4-DQ8/DR3-DQ2, recruited throughout Norway during 2001-2007). We retrospectively tested blood samples taken at age 3, 6, 9, and 12 months, and then annually, to determine when TG2 antibodies developed. Of 220 genetically at-risk children tested, 25 were diagnosed with CD (cases; ESPGHAN 2012 criteria) and matched for follow-up time, birthdate, and county of residence with 2 randomly selected children free from CD (controls) from the cohort. Viruses were quantified in monthly stool samples (collected from 3 through 35 months of age) using real-time polymerase chain reaction methods. RESULTS: Parechovirus was detected in 222 of 2,005 stool samples (11.1%) and was more frequent in samples from cases before developing TG2 antibodies (adjusted odds ratio 1.67, 95% confidence interval 1.14-2.45, P = 0.01). The odds ratio was higher when a sample was positive for both parechovirus and enterovirus (adjusted odds ratio 4.73, 95% confidence interval 1.26-17.67, P = 0.02). Anellovirus was detected in 1,540 of 1,829 samples (84.2%), but did not differ significantly between case and control subjects. DISCUSSION: Early-life parechovirus infections were associated with development of CD in genetically at-risk children.
Department of Chronic Diseases and Ageing Norwegian Institute of Public Health Oslo Norway
Department of Pediatric Research Oslo University Hospital Oslo Norway
Department of Pediatrics Østfold Hospital Trust Grålum Norway
References provided by Crossref.org
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- $a Tapia, German $u 1Department of Chronic Diseases and Ageing, Norwegian Institute of Public Health, Oslo, Norway; 2Department of Paediatric, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic; 3Department of Pediatrics, Østfold Hospital Trust, Grålum, Norway; 4Department of Pediatrics, Institute of Clinical Sciences, The Sahlgrenska Academy at University of Gothenburg and Queen Silvia Children's Hospital, Gothenburg, Sweden; 5Division of Institute Resources, Department of IT and e-health, Norwegian Institute of Public Health, Oslo, Norway; 6Department of Pediatric Research, Oslo University Hospital, Oslo, Norway
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- $a INTRODUCTION: To test whether parechovirus and anellovirus, frequent enteric viruses, were associated with subsequent celiac disease (CD). We hypothesized that children who later developed CD would have increased frequency of parechovirus infections before transglutaminase 2 (TG2) antibody development. Anellovirus testing was exploratory, as a potential marker of immune status. METHODS: Matched case-control design nested within a longitudinal birth cohort (the MIDIA study) of children at genetic risk of CD (carrying the human leukocyte antigen genotype DR4-DQ8/DR3-DQ2, recruited throughout Norway during 2001-2007). We retrospectively tested blood samples taken at age 3, 6, 9, and 12 months, and then annually, to determine when TG2 antibodies developed. Of 220 genetically at-risk children tested, 25 were diagnosed with CD (cases; ESPGHAN 2012 criteria) and matched for follow-up time, birthdate, and county of residence with 2 randomly selected children free from CD (controls) from the cohort. Viruses were quantified in monthly stool samples (collected from 3 through 35 months of age) using real-time polymerase chain reaction methods. RESULTS: Parechovirus was detected in 222 of 2,005 stool samples (11.1%) and was more frequent in samples from cases before developing TG2 antibodies (adjusted odds ratio 1.67, 95% confidence interval 1.14-2.45, P = 0.01). The odds ratio was higher when a sample was positive for both parechovirus and enterovirus (adjusted odds ratio 4.73, 95% confidence interval 1.26-17.67, P = 0.02). Anellovirus was detected in 1,540 of 1,829 samples (84.2%), but did not differ significantly between case and control subjects. DISCUSSION: Early-life parechovirus infections were associated with development of CD in genetically at-risk children.
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