Virus linked to food sensitivity

Celiac disease is a digestive disorder that’s triggered by eating foods containing gluten—a protein common in foods. When a person with celiac disease eats or drinks anything with gluten, the body’s immune system attacks the inside of the small intestine. The damage from this attack keeps the body from absorbing needed nutrients. If left untreated, celiac disease can lead to malnutrition, anemia, weakened bones, and other problems.

Reovirus core. Image credit: Jawahar Swaminathan/European Bioinformatics Institute (PD)

Researchers don’t know exactly what triggers celiac disease. Certain genes and other factors, such as things in the environment, can lead to celiac disease. Viral infections have been suggested as a possible trigger.

A team from the University of Chicago and the University of Pittsburgh School of Medicine investigated whether a common but harmless type of virus that people are frequently exposed to, called reoviruses, can prompt sensitivity to dietary proteins.

They studied two different strains of reoviruses (T1L, which can infect the intestine, and T3D-RV, which was engineered to infect the intestine) in mice. Both strains triggered an immune response that protected the mice against the infection.

However, animals infected with TL1 also showed altered immune responses in the gut. Both type 1 interferon (IFN) signaling and interferon regulatory factor 1 (IRF1) expression increased.

IRF1 regulates gene transcription and plays a key role in oral tolerance, or the suppression of immune responses to an orally delivered substance, like food. After being infected with T1L, susceptible mice lost their oral tolerance to a dietary protein.

A follow-up gene expression analysis showed this was triggered by specific changes in immune signaling molecules. These changes both block the mechanism that maintains tolerance to dietary proteins and promote the immune reaction against them.

Patients with celiac disease had higher levels of reovirus antibodies than controls. Patients on a gluten-free diet also had higher levels of reovirus antibodies and IRF1 levels in their small intestines, suggesting reovirus infection may lead to long-lasting gene expression changes. (NIH)

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