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Evidence Emerges That Celiac Disease Could Be Triggered by a Seemingly Harmless Virus

And we might be able to vaccinate against it.

FIONA MACDONALD
6 APR 2017
 

Researchers have found early evidence that a common but harmless virus could be behind the incurable celiac disease, by causing our immune systems to turn against gluten.

Up until now, research has mainly focussed on the idea that celiac is a genetic disease, but this new study suggests that early infection with a virus called the reovirus could also play a role. The good news is that, if the infection hypothesis is confirmed, it could lead not only to much-needed new treatment options, but potentially even a vaccine.

 

Celiac disease is an autoimmune condition where the immune system starts attacking the lining of a patient's small intestine every time it's exposed to even the tiniest amount of gluten.

While many people who claim gluten intolerance don't actually have celiac disease, it's still a big problem for hundreds of thousands of people - one in 133 people in the US alone experience the condition, and researchers estimate that only 17 percent of those who have the condition in the country have actually been diagnosed.

There's currently no cure or effective treatments, and the only way to manage it is to cut out gluten entirely - not just by avoiding wheat-based bread and pastas, but choosing gluten-free toothpastes, soy sauces, and many other household products.

Previous research had found links between viral infections and celiac, but this is the first time researchers have been able to experimentally confirm the link, showing how a common and harmless human strain of reovirus could trigger celiac disease in mice.

The results need to be replicated in humans, but it's part of a growing body of evidence that suggests autoimmune diseases such as celiac disease and type 1 diabetes don't arise on their own, but are influenced by the presence of outside pathogens.

That's not to say an infection on its own is enough to trigger the disease, but combined with genetic factors could be playing a previously ignored role in bringing about the condition - particularly if infection occurs around the same time babies are exposed to gluten in their diet.

 

"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 lead researcher Bana Jabri from the University of Chicago Celiac Disease Centre.

"However, the specific virus and its genes, the interaction between the microbe and the host, and the health status of the host are all going to matter as well."

Gluten's a dietary protein that's found in many modern grains, and our body struggles to digest it, which means it's more likely than other proteins to trigger allergies or an immune response.

But despite the fact that claims of celiac disease increased up to four-fold between 1990 and 2011 in some parts of the world, scientists still don't fully understand how and why some people's immune systems trigger such a strong inflammatory response to gluten - and why it's becoming more common.

"The results are of great interest considering the recent increase in prevalence of food allergies and autoimmune disorders, which suggests an unknown environmental risk modifier," Elena F. Verdu and Alberto Caminero from McMaster University in Canada, who weren't involved in the research, write in a perspectives piece in Science accompanying the research.

To figure out whether the common but harmless human reovirus could be playing a part in this increase, Jabri and her colleagues took two different reovirus strains that infect humans, type 1 Lang (T1L) and type 3 Dearing (T3D), and tested them on mice.

They found that both T1L and T3D could trigger protective immune responses - activating the immune system to attack anything foreign it can find - but only T1L caused the mice's immune systems to act against gluten, triggering a celiac-like condition.

Interestingly, the T1L virus triggered an immune response that was dependent on one molecule in particular, Interferon regulatory factor 1 (IRF1) which earlier studies have found at higher than normal levels in the small intestines of children with celiac disease.

These results now need to be verified in humans, but suggest that people who become infected with T1L could be more likely to experience and immune response against gluten, even when they have no other side effects.

"We have been studying reovirus for some time, and we were surprised by the discovery of a potential link between reovirus and celiac disease," said one of the researchers, Terence Dermody from the University of Pittsburgh School of Medicine.

"We are now in a position to precisely define the viral factors responsible for the induction of the autoimmune response."

The researchers then took things one step further, and looked at 73 people without gluten intolerance and 160 people with celiac disease, and showed that the celiac patients had much higher levels of reovirus antibodies and IRF1 gene expression than the control group

According to the team, this suggests that infection with a reovirus could leave a permanent mark on the immune system that sets the stage for a later autoimmune response to gluten.

They hypothesise that it's most likely that children would be infected with the reovirus around the same time gluten is introduced to their diet, which could trigger the condition - and they plan to test this idea in future studies.

If it's verified in future studies, it means a simple vaccine might be enough to protect children from gluten intolerance later in life.

"During the first year of life, the immune system is still maturing, so for a child with a particular genetic background, getting a particular virus at that time can leave a kind of scar that then has long term consequences," said Jabri.

"That's why we believe that once we have more studies, we may want to think about whether children at high risk of developing celiac disease should be vaccinated."

The research has been published in Science

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