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Children with the intestinal virus, the enterovirus, are at increased risk of later developing celiac disease.
A new study, published in The bmj, found that enterovirus in early childhood may be a trigger for celiac disease in children at increased genetic risk of celiac disease
However, the adenovirus, another common virus, was not badociated with a risk of subsequent celiac disease.
This preliminary discovery adds new insights into the role of viral infections as a potential underlying cause of celiac disease, say the researchers.
Celiac disease is a common digestive condition caused by an adverse reaction to gluten, a dietary protein found in wheat, barley and rye. It is thought that it develops from a combination of genetic and environmental triggers.
Previous studies suggest that stomach and bowel infections, common in childhood, play a role in the development of celiac disease. But no firm conclusion has been made.
The researchers therefore tested whether enterovirus and adenovirus infections – before the development of celiac disease antibodies – were more common in children diagnosed with celiac disease later than in others.
Between 2001 and 2007, they recruited 220 Norwegian children with the genetic makeup HLA DQ2 and DQ8. The vast majority of patients with celiac disease are carriers of at least one of them, which increases the risk of celiac disease and type 1 diabetes.
Researchers collected stool samples aged 3 to 36 months to detect viruses, and blood samples were tested for antibodies to celiac disease at 3, 6, 9, and 12 months, and once a year until 2016.
After an average of nearly 10 years, 25 children were diagnosed with celiac disease. Each child was then paired with two healthy witnesses.
The enterovirus was detected in 370 (17%) of the 2135 stool specimens, in 73 children with at least one positive sample. And it was significantly more common in samples taken before the development of antibodies to celiac disease in cases than in controls – 84 out of 429 (20%) and 129 out of 855 (15%) in controls.
There was a significant badociation between exposure to the enterovirus and the subsequent risk of developing celiac disease, but the adenovirus was not related to the development of the disease.
Enterovirus infections contracted after the introduction of gluten into the child's diet were badociated with celiac disease, whereas those before or at the time of introduction were not, suggesting that she herself was the trigger of the disease.
This is an observational study. Therefore, no definitive conclusion can be drawn as to the cause and researchers can not exclude the possibility that other unmeasured factors may have influenced the results. In addition, the number of children with celiac disease was limited and the results may not be generalized to broader genetic profiles.
But the authors point out that it is the first study of its kind to explore the link between viruses in childhood and subsequent celiac disease.
In addition, the constitution of the gene HLA-DQ2 or HLA-DQ8 represents almost all people "genetically predisposable". Therefore, they believe that their findings will likely apply to a large proportion of those suffering from celiac disease.
With nearly 40% of the population genetically predisposed to celiac disease, the authors point to the "major problem" of identifying environmental triggers.
The authors suggest that identifying specific viruses as triggers may warrant preventative strategies: "If the enterovirus is confirmed as a triggering factor, vaccination could reduce the risk of developing celiac disease," conclude -they.
