In the United States, approximately 1 in every 133, or at total of 2 million people, have celiac disease. The condition, in which the immune system reacts to the ingestion of the protein gluten, can cause permanent intestinal damage when left untreated.
While the exact cause of celiac is unknown, there are several factors that may contribute to the condition, including genetics, environment, infant feeding practices, and gut bacteria. Most recently, the role of being infected with viruses that go on to trigger the condition is being studied.
Rotavirus is the most common cause of intestinal illness in children, with symptoms including abdominal pain, vomiting, severe watery diarrhea, and fever. Previous research — done almost 10 years ago — noted the increase in the development of celiac disease in patients who were infected with rotavirus.
While further mechanisms need to be studied, these initial studies pointed to the role of specific viruses and their ability to activate immune responses that trigger celiac disease in susceptible individuals.
There is a vaccine now available for rotavirus that protects about 90 percent of vaccinated children from severe illness and 70 percent from the illness completely. It will be interesting to see if the vaccine will play a role in the number of new celiac cases over time.
Reovirus is an infection that is generally asymptomatic in humans, so its role in the development of celiac disease is especially interesting. A 2017 University of Chicago and the University of Pittsburgh School of Medicine study published in Science looked at two reovirus strains and how they triggered celiac in mice that were genetically predisposed to the condition.
Researchers found that one of the strains, known as T1L, triggered the celiac while the other strain, T3D (which was generically different from T1L), did not trigger disease development. This study went further than its predecessors by determining that there were two ways the virus triggered celiac disease development — suppressing the formation of regulatory immune cells and promoting and inflammatory response to gluten.
Future studies will need to look at determining when this infection occurs (due to the usual lack of symptoms), whether the timing of the infection may also play a role, and how those things interact with other factors to contribute to disease development.
Other viruses have also been linked with celiac disease, such as hepatitis C, though more recent research showed no link between the two. Future research will be needed to see which, if any, additional viral infections (and the specific strain) may play a role in celiac disease.
The mechanisms in which the viral infections effect the immune system, boosting the immune systems of susceptible persons, and vaccinating against these specific viral infections in those with a genetic risk of developing celiac disease could be the keys to preventing the disease in the future.
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