Viral infections have been the focus of attention in the development of autoimmune diseases—diseases where the body's immune system reacts to the body's own cells—because they trigger the immune system into action.
In a study published in Science, led by senior author Dr. Bana Jabri from the Celiac Disease Center at the University of Chicago, reported that infection with reovirus, a common harmless virus, can trigger an immune system response to gluten that leads to celiac disease, an autoimmune disease of the small intestine.
The scientists found celiac disease patients had much higher levels of antibodies against reoviruses than those without the disease, indicating a present or past infection with the virus. Patients with high reovirus antibodies also had much higher levels of IRF1 gene expression, a protein that plays a key role in the loss of tolerance to gluten, a tolerance that most of us have.
The researchers used two different reovirus strains to show how genetic differences between viruses can change how they interact with the immune system. When given to mice, both reovirus strains induced a protective immune response to the virus, but did not cause overt disease.
One common human reovirus, however, triggered the immune system to generate inflammation—a process seen in people with celiac disease where cells of the immune system gather and release chemicals in response to infection—and the loss of oral tolerance to gluten. The other closely related, but genetically different strain did not.
What's particularly novel about this research is the finding that the infection with reovirus could have occurred earlier and set up the immune system reaction that leads to 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 Jabri in a press release from the University of Chicago Medical Center.
People with celiac disease can't eat gluten—found in wheat, rye, and barley—because the response mounted by their immune system damages their small intestine. They have to be aware of unusual sources of gluten, like medicines, vitamins and supplements, lip balm, and glue on stamps and envelopes.
Celiac disease is not the same as a wheat allergy. People with a wheat allergy might have itchy eyes and trouble breathing, but they do not have damage to their small intestine.
The inflammation caused by the immune system's reaction to gluten damages the lining of the small intestine by flattening the finger-like projections, called villi. The mucosal lining of the intestine can become leaky and allow water and salts to leak out of the cells and be lost with diarrhea.
About one in 100 people in the US have the disease, and women with celiac disease outnumber men by two to one.
Certain genes predispose people to getting celiac disease. More people with a protein called HLA DQ2 or DQ8 on their cells get celiac disease and the genes coding for these proteins can be inherited. These HLA types are present in 98.4% of celiac patients, but only 55.4% of people from the general population without celiac disease in the family.
The environment also seems to play a role because there is a high frequency in Finland, but low in Russia—and people are genetically similar in the two countries.
The symptoms of celiac disease vary from person to person. Some people have digestive symptoms, such as bloating, diarrhea, constipation, nausea, gas, and stomach pain. Children with celiac disease may have delayed physical development, weight loss, and loss of enamel on permanent teeth, but irritability is the most common symptom in kids.
Sticking to a strict gluten-free diet is the only treatment for celiac disease. Symptoms usually start to improve within weeks in adults and three to six months in children. And once the damage to the intestine heals, nutrients can be effectively absorbed from the intestine again.
For some, a life without bread can be tough. Of course, it's critical for treating the disease, but how much better would life be if we could figure out how to prevent celiac disease altogether?
The study by Jabri and colleagues reinforces the importance of looking at immune responses to viruses—even after an infection clears—not just the infection itself, as a way to investigate the development of autoimmune diseases, like celiac.
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