Typically Harmless Virus May Trigger Celiac Disease

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A usually harmless virus may play a role in triggering celiac disease, a new study in mice suggests.

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. This immune response is similar to what's seen in people with the condition.

Although human infections with reoviruses are common, the viruses don't cause symptoms in people. But the study also found that patients with celiac disease did have higher levels of antibodies against reovirus, compared to people without the condition.

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.

"A virus that is not clinically symptomatic can still do bad things to the immune system and set the stage for an autoimmune disorder," such as celiac disease, study co-author Dr. Bana Jabri, director of research at the University of Chicago Celiac Disease Center, said in a statement.

The researchers also found people with celiac disease who had high levels of reovirus antibodies also had increased expression of a gene that encodes a protein called IRF1. In the mouse studies, the researchers saw that IRF1 played a role in developing gluten intolerance after reovirus infection.

However, the researchers noted that only one particular strain of reovirus, called T1L, triggered the immune responses seen in the study. It's not clear if other types of reovirus have the same effect, they said. The other strain they tested, called T3D, is genetically different from T1L, and did not trigger the immune response.

In addition, other factors besides reovirus infection, such as a person's genes and their overall health, would likely play a role in whether the virus triggers celiac disease, the researchers said. [5 Ways Gut Bacteria Affect Your Health]

Celiac disease is an autoimmune disorder in which people's immune systems react abnormally to the protein gluten, which is found in wheat, rye and barely, and this reaction damages the lining of the small intestine. The condition affects about 1 out of every 100 people in the United States.

Previous studies have suggested a link between infections with certain viruses, including hepatitis C virus, and rotavirus (a virus in the same family as reovirus) and the development of celiac disease. However, evidence showing exactly how any virus might trigger the disease is lacking.

The study showed that T1L acted in two ways: It suppressed the formation of certain types of "regulatory" immune cells that usually allow the body to know that it shouldn't attack certain substances. And it also promoted an inflammatory response to gluten.

The researchers noted that although their study showed that reovirus infection led to an immune reaction against gluten, this reaction alone wouldn't damage to the small intestine. There are more steps that need to occur before the body experiences damage to the small intestine, and the study did not look at these steps.

More studies are also needed to determine if the timing of a reovirus infection with regard to initiation of gluten in the diet plays a role in the development of celiac disease, Dr. Elena F. Verdu, and Alberto Caminero, of McMaster University, Hamilton, Canada, wrote in a commentary accompany the study.

The study and commentary are published today (April 6) in the journal Science.

Original article on Live Science.

Rachael Rettner

Rachael is a Live Science contributor, and was a former channel editor and senior writer for Live Science between 2010 and 2022. She has a master's degree in journalism from New York University's Science, Health and Environmental Reporting Program. She also holds a B.S. in molecular biology and an M.S. in biology from the University of California, San Diego. Her work has appeared in Scienceline, The Washington Post and Scientific American.