The onset of celiac disease, an autoimmune disorder marked by a sensitivity to gluten, may be trigged by a typically symptomless viral infection many people contract in childhood, new research suggests.
Scientists don’t known exactly what causes celiac, but it’s likely a confluence of genetic and environmental factors. The Mayo Clinic estimates that celiac affects only about 1 percent of the population in Western countries, even though about 30 percent of Americans carry a gene that predisposes them to the disease. There’s also evidence to suggest that a significant proportion of people with celiac are undiagnosed and unaware they have the disease.
Reovirus might trigger the immune response that leads to celiac disease, according to a study published Friday in the journal Science. (Although a portion of the study was in mice rather than humans, the results provide growing evidence to support the theory that viruses can disrupt the body’s immune system.)
“It’s very important to do human studies, but also to have animal models to establish cause-effect relationships,” Dr. Bana Jabri, director of research at the University of Chicago Celiac Disease Center and co-author of the new study, told The Huffington Post.
“What one needs is actually to go back and forth between findings, from human to mouse and mouse back to human,” she said.
Jabri’s study had two phases. In phase one, the researchers genetically engineered mice to be susceptible to celiac disease, then exposed them to human reovirus and fed them gluten. The mice’s inflammatory immune response to the gluten was comparable to what’s seen in humans with celiac disease.
Phase two of the study analyzed patients with celiac disease and found that individuals with celiac had higher levels of antibodies against reovirus than the control population.
The theory that an infection can trigger an autoimmune disorder existed before this study. The new research, however, is “the first tractable experimental model to tackle this question,” Julie Pfeiffer, associate professor of microbiology at University of Texas Southwestern, told NPR.
“More studies in humans are warranted,” noted Pfeiffer, who was not involved in the research.
Prevention is crucial for people who don’t have celiac disease but who carry the gene for it.
“When a disease develops, it’s never from one day to the other,” Jabri said. “It’s like a cancer. When somebody starts to have a tumor that they can touch, things have been happening for years. It’s the same thing for autoimmune disorders.”
Understanding celiac triggers is a step toward prevention.
Celiac disease is an autoimmune disorder that prompts a reaction in the small intestine when a person eats gluten, a protein often found in wheat, rye and barely. The immune reaction prevents the body from absorbing nutrients; over time, it damages the small intestine’s lining and can cause diarrhea, fatigue, weight loss, bloating and anemia. Children with celiac disease can have growth and development problems.
There is no cure for celiac disease, but following a strict gluten-free diet can ease symptoms.
Gluten can be difficult to digest, even in people who don’t have celiac disease. Some people who test negative for the disease may have what’s known as non-celiac wheat sensitivity, which can cause diarrhea, stomach pain, bloating and altered mood.
For individuals with a family history of celiac disease, research into the disorder’s development is a promising first step toward prevention. However, preventative care is difficult because celiac may be multiple diseases ― meaning no one cure or prevention method would work for everyone.
Still, if further research confirms the theory that reovirus is indeed a celiac trigger, the next step could be developing a vaccine against the virus.
“That’s very feasible,” Jabri said.
CORRECTION: A previous version of this article stated that celiac disease is marked by an insensitivity to gluten. In fact, celiac is marked by gluten sensitivity.
This reporting is brought to you by HuffPost’s health and science platform, The Scope. Like us on Facebook and Twitter and tell us your story: firstname.lastname@example.org.