A research study published in the journal, Science, may have established a link between reovirus and celiac disease. Although reovirus is considered a common and often harmless virus, the study, co-authored by CDF Medical Advisory Board member, Stefano Guandalini, MD, and CDF Research Committee member, Sonia Kupfer, MD, determined that the reovirus, T1L, in some cases, might be causing the immune system to attack harmless food molecules, like gluten, triggering celiac disease. The study also found that celiac disease patients had more anti-reovirus antibodies compared to people without celiac disease. Celiac Disease Foundation Chief Executive Officer, Marilyn G. Geller, was quoted in this Gizmodo article about the finding.
Celiac disease is a serious, genetic, autoimmune disease caused by an immune reaction to the ingestion of gluten. Approximately 40% of the population has one or both genetic biomarkers for celiac disease, but just 1% of the population actually develops the disease at some point in their life. Researchers have yet to discover why the immune response to gluten activates in some people who are genetically predisposed, but not in others.
More research is necessary not only to determine if there are other viruses in addition to reovirus that may link to celiac disease, but also to understand more fully this possible link between reovirus and celiac disease. These findings would have future implications for celiac disease treatments and a cure. For example, if future research determines that reovirus is, in fact, a direct trigger for celiac disease, “then a reovirus vaccine could be developed for at-risk children, which could potentially block the development of celiac disease.¹” Celiac Disease Foundation is committed to keeping you informed on this and all other celiac disease research.
Read the original study here.
¹Eaton, Elizabeth (2017, April 6). Common virus may be celiac disease culprit.
Sciencenews.org. Retreievd from: https://www.sciencenews.org/article/common-virus-may-be-celiac-disease-culprit?ncid=newsltushpmgnews