A symptom-free virus may spark allergy to gluten

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In a new study, researchers have found that infection with reoviruses might play a role, a finding that might bring us closer to a vaccination against celiac disease.

"If confirmed by clinical studies, this link between celiac disease and reovirus is exciting because it identifies a possible target for vaccine prevention", said Alessio Fasano, a pediatric gastroenterologist who studies celiac disease at the Massachusetts General Hospital for Children in Boston and who was not involved in the work. "However, the specific virus and its genes, the interaction between the microbe and the host, and the health status of the host are all going to matter as well".

Celiac disease is an autoimmune disorder that affects an estimated 300,000 people in Canada, although many of them have not been officially diagnosed.

Celiac disease is caused by an abnormal immune response to the protein gluten, which is found in wheat, rye and barley.

Dermody doesn't think that the T1L reovirus is the only virus that can stimulate celiac disease. More specifically, the virus primes their immune systems to shut down regulatory cells that hold back overly aggressive immune responses. But for those with celiac disease, the inflammatory response can lead to destruction of the lining of the small intestine, potentially leading to death.

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Celiac disease is not an eating disorder, but may pose similar symptoms to anorexia, including weight loss and fatigue. Both reovirus strains induced protective immunity and did not cause overt disease.

The researchers found that, among mice that were genetically engineered predisposed to celiac disease, those that were infected with a virus called reovirus were more likely to have an immune response against gluten than mice not infected with a reovirus.

"We are now in a position to precisely define the viral factors responsible for induction of the autoimmune response".

But they found another piece of evidence: Humans with celiac disease seem to have a higher level of the antibody, or pathogen-killing protein, for reovirus-which seemed to imply some sort of earlier viral exposure.

Additionally, the analysis revealed that a higher level of reovirus antibodies was associated with increased expression of the IRF1 gene, which is a key player in the loss of oral tolerance to gluten.

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The findings suggest that reovirus infection may leave a "permanent mark" on the immune system that sets the body up for developing celiac disease, the researchers said. But now, a large global team of researchers has presented some convincing evidence that the story goes deeper than that-the disease's trigger might lie in a benign viral infection.

"During the first year of life, the immune system is still maturing, so for a child with a particular genetic background, getting a particular virus at that time can leave a kind of scar that then has long-term consequences", Jabri said.

Most infants eat their first gluten-containing cereals around six months of age, a time when their immune systems are more vulnerable to viruses. Epidemiological studies suggest there's a connection between viral infections during childhood and development of celiac later in life, but scant experimental evidence connects the two. This could be because the others haven't been exposed to a viral trigger.

New evidence for how childhood infections could trigger ciliac disease.

I've reached out to a few doctors and folks from the Celiac Disease Foundation for an outside comment-one major caveat is the fact that the study was in mice, and effects in mice might not translate to effects in humans.

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"We have been studying reovirus for some time, and we were surprised by the discovery of a potential link between reovirus and celiac disease", said Dr. Terence Dermody, co-author of the study and chair of the University of Pittsburgh School of Medicine's department of pediatrics, in a press release.

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