Thursday , June 17 2021

Common virus can cause celiac disease in children



Common virus can cause celiac disease in children

Children who are affected by the common intestinal virus, enterovirus, are at increased risk for later celiac development.

A new study, published in BMJ, found that early childhood enterovirus could be a cause of celiac disease in children with increased genetic risk of the disease.

However, adenovirus, another common virus, is not associated with the risk of later Celiac disease.

This preliminary conclusion adds new information about the role of viral infections as a potential root cause of celiac disease, researchers say.

Celiac disease is a common digestive tract caused by an unwanted reaction to gluten, a protein that is contained in wheat, barley and rye. It is believed to evolve from a combination of genetics and ecological triggers.

Previous studies have shown that gastric and intestinal infections, which are common in childhood, play a role in the development of celiac disease. But no definite conclusions were made.

So the researchers tested whether enteroviral and adenovirus infections – before the development of antibodies to celiac disease – were more common in children who were later diagnosed with celiac disease than those who were not.

Between 2001-2007, they recruited 220 children from Norway who carried both HLA DQ2 and DQ8 genetics. The vast majority of celiac patients wear at least one of them, which carries an increased risk of celiac disease and type 1 diabetes.

Researchers collected stool samples from 3 to 36 months of age to detect viruses, and blood samples were tested for celiac antibodies at 3, 6, 9 and 12 months, and then annually until 2016.

After an average of about 10 years, 25 children were diagnosed with celiac disease. Then each child is matched with two healthy controls.

Enteroviral was found in 370 (17%) of 2135 stool samples, with 73 children having at least one positive sample. It was much more common in samples collected prior to the development of antibodies to celiac disease in cases than in controls – 84 out of 429 (20%) in the cases and 129 out of 855 (15%) in the controls.

There is a significant association between enteroviral exposure and later on the risk of celiac disease, but the adenovirus is not related to the development of the disease.

Enteroviral infections caught after gluteal insertion in the child's diet are associated with celiac disease, whereas those before or during administration were not, suggesting that the infection itself is the cause of the disease.

This is an observational study, so hard conclusions can not be made about the cause, and researchers can not rule out the possibility that other incalculable factors may have affected the results. Moreover, the number of children with celiac disease is limited and the findings can not be summed up for broader genetic profiles.

But the authors point out that this is the first study of its kind to explore the link between viruses in childhood and later celiac disease.

And the structure of HLA-DQ2 or HLA-DQ8 represents almost all of the "genetically susceptible" people, so they believe that their findings are likely to apply to a large proportion of celiac patients.

Since nearly 40% of the population is genetically predisposed to celiac disease, the authors highlight the "main problem" in identifying environmental factors.

The authors suggest that identifying specific viruses such as triggers can justify preventative strategies: "If enterovirus is confirmed as a triggering factor, vaccination may reduce the risk of celiac development," they conclude.

Image Credits: © stock.adobe.com / au / Roman Janushevski