This is the first time that a link has been discovered between the inflammatory bowel disease and enteroviruses, which are a genus of positive-sense single-stranded RNA viruses.
The finding was published in the international journal Clinical and Translational Gastroenterology.
One of the authors of the study, Alkwin Wanders, at Uppsala University and Uppsala University Hospital, believes that the results could help better understand the root causes of Crohn's disease.
Not much is known about what causes Crohn's disease; there have been over 140 gene mutations associated with condition. Most of the genes that have been identified play a role in immune defense.
Hence, there have been many theories suggesting that the condition could be caused by a lack of immune defense against various different pathogens, which would mean that Crohn's disease is a result of both environmental and genetic factors.
Researchers at McGill University and Génome Québec Innovation Centre, along with scientists from other Canadian and Belgian institutions, discovered there are DNA variations in a gene that increase susceptibility to developing Crohn's disease. Their finding was published in Nature Genetics.
Crohn's diseases is characterized by inflammation of the digestive tract, affecting different parts of the gut, from the mouth down to the anus. Symptoms include: severe stomach ache, weight loss, strictures in the intestines and diarrhea.
The genes associated with the onset of the condition are vital for the immune defense against a certain type of RNA virus.
An interdisciplinary research team in Sweden set out to determine whether this type of virus might be linked to a higher risk of developing Crohn's disease. They wanted to see whether a cohort of patients with Crohn's disease had RNA viruses. They focused particularly on a group of RNA viruses called enteroviruses - which infect the intestinal mucous lining.
The team found that children suffering from Crohn's disease had significantly higher numbers of enteroviruses in their intestines compared to those in the control group - without Crohn's disease.
The scientists also identified enteroviruses in nerve cell ganglia (in deeper parts of the intestinal wall). In addition, receptors for a group of enteroviruses were found in the intestinal mucous linings and nerve cell ganglia, which gives insight into how the virus enters the system of nerves in the intestine.
Interestingly, they also found that enteroviruses are also be stored in nerve cells in the intestine and then spread via nerve fibers to other parts of the intestine.
Alkwin Wanders, said that this would explain the periodic nature of the disease.
The study included a total of nine children with advanced Crohn's disease as well as fifteen with incipient symptoms of the disease. The investigators said that there needs to be further research conducted on a larger group of patients to fully understand the link.
The authors said the results from this study "show, for the first time, significant presence of HEV-B in the mucosa and enteric nervous system of patients with ileocecal Crohn's disease (ICD)."
Our data should be put in perspective of what others have found and discussed in terms of a role of interplay between mutations in genes encoding proteins involved in innate viral immunity and autophagy, and the presence of microorganisms, both viruses and bacteria, as a triggering factor of Crohn's disease."
A previous study by scientists at Cornell University found that a novel group of E. coli bacteria is associated with intestinal inflammation in patients with Crohn's disease.
Written by Joseph Nordqvist