Researchers at the University of Pittsburgh have discovered that a seemingly harmless virus might be a trigger for celiac disease.
Reovirus infects most humans within the first five years of life, according to Dr. Terry Dermody, Chair of Pediatrics at the University of Pittsburgh School of Medicine.
But Dermody said the virus is typically innocuous; even an infant’s immune system can mount an effective response.
Dermody said he's studied reovirus for more than 20 years in his lab at Pitt and discovered that it caused a strong immune response in mice.
He coupled that knowledge with the hypothesis that there must be some sort of trigger that causes people to develop celiac disease, since about one-third of the population carries the gene that makes them vulnerable to celiac, but less than 1 percent of people actually have the disease. Celiac disease is characterized by an autoimmune response to the ingestion of gluten, which damages the small intestine and prevents nutrient absorption.
“That must mean that there’s something in the environment that serves as a trigger to cause celiac disease in those people who are at risk,” Dermody said.
When Dermody’s team infected mice with a particular strain of reovirus at the same time they introduced gluten to the rodents’ diet, they saw a celiac-like immune response. Another closely related strain of reovirus did not cause such a response.
Dermody hypothesized that something similar might be happening in humans, when parents give their babies wheat products in the first year or two of life.
“If it’s the right genetic pre-disposition," Dermody said. "If the virus goes in at the same time the gluten goes in, the immune system is tricked and thinks that … the gluten is a dangerous substance that should lead to a vigorous immune response, just like a virus would."
Dermody said they also found that the blood of people people with celiac disease tended to have more anti-bodies for reovirus than people without celiac, suggesting their bodies had at one point mounted a substantial immune response against the virus.
But he said not every celiac patient studied had high levels of reovirus antibodies, which means there could be multiple triggers for development of the disease.
“What we want to be able to do is define the percentage of people with celiac disease in which reovirus was a trigger, and we’d like to also know what other triggers would be common,” Dermody said.
The study, done in collaboration with researchers at the University of Chicago, is published in the latest issue of the journal Science.