Celiac Disease Induced By Common Virus: Study

Catching a common virus that’s otherwise harmless may provoke an immune response that mimics celiac disease, according to a new study on mice.

When given to mice, an infection known as reovirus sparked an inflammatory response that led the immune system to “overreact” to gluten and essentially bring on celiac disease.

The researchers, reporting from the University of Pittsburgh and University of Chicago, believe that the new study should alert the medical community to previously unchecked causes of autoimmune disorders, including celiac disease.

“This study clearly shows that a virus that is not clinically symptomatic can still do bad things to the immune system and set the stage for an autoimmune disorder, and for celiac disease in particular,” said study senior author Dr. Bana Jabri, professor in the department of Medicine and Pediatrics and Director of Research at the University of Chicago Celiac Disease Center.

The new study, however, falls short of ascribing the reovirus a full-on designation of disease inducer, even though it has shown to trigger celiac disease in particular cases. While the reovirus demands further study, so do the various factors at play in disease progression.

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“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,” said Jabri.

In certain cases, the reovirus may be “a key initiating event” for the development of celiac disease, a gluten-intolerance disorder that affects approximately one in 133 people in the United States. People with celiac disease are unable to process gluten, found in wheat, rye and barley products, and suffer intestinal damage when they consume it.

A Surprise Cause

While the researchers found that one strain of reovirus provoked an inflammatory response in the mice studies, a separate strain that was genetically different did not result in the same effects. Pinpointing the exact strain of virus associated with celiac disease should help bolster future treatment modalities.

“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, Chair of the department of Pediatrics at the Pitt School of Medicine. “We are now in a position to precisely define the viral factors responsible for the induction of the autoimmune response.”

In addition to the mice studies, the researchers also assessed levels of reovirus antibodies among people with celiac disease and found that higher antibody amounts were linked to increased levels of a gene expression tied to gluten tolerance.

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The research suggests that babies and young children who shift to eating solid foods containing gluten may face an increased risk of developing celiac disease if they acquire a reovirus 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.

“That’s why we believe that once we have more studies, we may want to think about whether children at high risk of developing celiac disease should be vaccinated.”