A new study raises a novel idea about what might trigger celiac disease, a condition that makes patients unable to tolerate foods containing gluten.

The study suggests that a common virus may be to blame.

For people with celiac disease, gluten can wreak havoc on their digestive systems. Their immune systems mistake gluten as a dangerous substance.

Scientists have known for a while that genetics predisposes some people to celiac. About 30 percent of Americans carry the genes that make them more susceptible to the disease. And yet, only about one percent of Americans have celiac.

Researchers wondered why not everyone with the risk genes gets the disease.

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The answer is likely complicated, but one theory has emerged. Perhaps a "viral infection can serve as a trigger to celiac," explains Dr. Terence Dermody, who chairs the Department of Pediatrics at the University of Pittsburgh, and is an author of the new study published in Science.

He and a team of collaborators, led by Bana Jabri of the University of Chicago, decided to test this in experimental mice. They had been studying reovirus – a common virus that infects most Americans beginning in childhood, yet isn't considered dangerous. The researchers genetically engineered the mice to be more susceptible to celiac disease. Then they exposed mice to reovirus. At the same time they also fed gluten to the mice.

It turns out their hunch had been right. The mice developed "an immunological response against gluten that mimics the features of humans with celiac disease," Dermody says. The symptoms of celiac disease include diarrhea and other signs of gastrointestinal distress.

"It's all about the timing," Dermody says. The idea is that when the virus and gluten are introduced at the same time, the immune system mistakes the gluten-containing food as dangerous.

Transmission electron micrograph of a cell infected with reovirus (red). The virus is very common and not considered dangerous. Scientists now think it may have a role to play in triggering celiac disease.

But could this be true in humans too?

The second phase of the new study suggests an answer. Dermody and his collaborators analyzed the antibody levels to various viruses in a group of people. They found people who have celiac disease have two- to five-fold higher levels of reovirus-specific antibodies.

"It's a clue that people who have celiac may have been exposed to reovirus before the development of their disease," Dermody says. But, he stresses that "it's just a clue."

It will take a long time to figure out if there's a causal link between reovirus infections and the onset of celiac disease. Dermody envisions a study involving thousands of children who would be followed for several years. For now, he and his collaborators have some grant funds from the National Institutes of Health to continue their research.

The upside of understanding this possible connection is significant, explains Dr. Bana Jabri, of the University of Chicago, who is a co-author of the new study.

If it's true that the virus can trigger celiac disease, then young children who carry the risk genes for celiac could be vaccinated against Reovirus. "It may be useful to start thinking about vaccinating people who are at a high risk of celiac disease against [these] types of viruses," she says.

Links between viral infection and the development of auto-immune disorders such as celiac disease have been proposed before, "but this is the first tractable experimental model to tackle this question," says Julie Pfeiffer, an Associate Professor of Microbiology at University of Texas Southwestern, who has followed the research, but is not involved in the new study. Given the interest and the findings, "more studies in humans are warranted," she says.

As awareness of celiac disease has grown, so too has the number of people experimenting with gluten-free diets due to concerns about gluten sensitivities. This is evident from the growth in gluten-free food sales and most recently, the introduction of gluten-free dining halls on two college campuses.

Copyright 2017 NPR.

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