Link shown between Crohn’s disease and virus

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Link shown between Crohn’s disease and virus

A new study reveals that all children with Crohn’s disease that were examined had a commonly occurring virus – an enterovirus – in their intestines. This link has previously not been shown for this chronic inflammatory intestinal disorder. The findings are being published today in the latest issue of the international journal Clinical and Translational Gastroenterology. These findings need to be confirmed in larger studies, but they are important, as this connection has never been pointed out before. This paves the way for a better understanding of what might be involved in causing the disease, says Alkwin Wanders, one of the scientists behind the study at Uppsala University and Uppsala University Hospital. In Sweden several thousand adults live with Crohn’s disease, and each year about 100 children and adolescents develop the disorder. The disease affects various parts of the gastrointestinal system and causes symptoms such as stomach aches, diarrhoea, and weight loss – in severe cases fistulas, or strictures in the intestines. The cause of Crohn’s disease is not known. Mutations in more than 140 genes have been shown to be associated with the disorder, but this genetic connection is not a sufficient explanation. Many of these genes play key roles in the immune defence, which has prompted theories that the disease might be caused by impaired immune defence against various microorganisms. In that case, the disease would be a consequence of interplay between heredity and environment. Recent research has shown that some of the genes that are strongly linked to the disorder are important for the immune defence against a certain type of viruses that have their genetic material in the form of RNA, so-called RNA viruses. Using this as a point of departure, an interdisciplinary research team was established in Sweden to investigate what role this type of virus plays in the disease. The research team includes the paediatrician Niklas Nyström, the pathologist Alkwin Wanders, virus researchers Gun Frisk and Oskar Skog, the molecular biologist Mats Nilsson, and the geneticist Ulf Gyllensten at Uppsala University and Uppsala University Hospital, along with cell biologists Jonas Fuxe and Tove Berg the paediatrician Yigael Finkel at Karolinska Institutet in Stockholm. This unique composition, with complementary clinical and scientific expertise, has been extremely fruitful for our studies, says Alkwin Wanders. In the present study the researchers investigated whether the RNA virus were present in children with Crohn´s disease. They focused in particular on the prevalence of enteroviruses, a group of RNA viruses that are known to infect the intestinal mucous lining. The results showed significant amounts of enteroviruses in the intestines of all of the children with Crohn´s disease, whereas the control group had no or only minimal amounts of enteroviruses in their intestines. Similar results were obtained using two different methods. Enteroviruses were found not only in intestinal mucous linings but also in so-called nerve cell ganglia in deeper segments of the intestinal wall. Receptors for a group of enteroviruses were also found in both the intestinal mucous linings and nerve cell ganglia, which may explain how the virus can make its way into the nerve system in the intestine. Another interesting finding is that the enterovirus could be thought to be stored in nerve cells in the intestine and to spread to different parts of the intestine via nerve fibres. This would explain both the fact that the disease is periodic (comes and goes) and the fact that it often affects multiple segments of the intestines, says Alkwin Wanders. The present study comprises nine children with advanced Crohn’s disease and fifteen children with incipient Crohn’s disease symptoms. The research now wants to go on to examine larger groups of patients and more control individuals. They also want to pursue experimental research to investigate the link further.
 
Maybe a bit too soon to say, but its sounding promising. Thanks for the link Igor
 
Ok, since I am swedish and I my GI is one of the professors at Uppsala, where they made this study, I asked him about it. This is what he answered:

"So far, we see virus in IBD as a passenger. No posetive outcome out of treatment results in viral treatment. Norovirus gives horrible diarrhea. It´s like turning on a tap."

I might go into more detail with him after my vacation, but what I find interesting about this GI is that he is soon performing studies looking at the "leakiness" of the intestine. I´ve signed up for it, but as you know USA and particulary Sweden have the most incidents of IBD which is scary as hell.
 
Whether it be stealth mycoplasma, accumulative metal poisoning (unfiltered water/vaccines/air pollution chemi-trail/exhaust/powerplant/incineration of hazardous trash), the myriad of intestinal ravaging food additives/sugars/fake sugars/GMOs/pesticides/herbicides, dirty cell lines in vaccines...that first damage the intestinal wall, an unending list of opportunistic viruses and bacteria certainly take root in the walls and multiply--which should be the target of therapy just as much as the immuno-modulating approaches. Additionally, diet contributes to or ameliorates such conditions in the digestive tract which harbor infections. All my off the cuff opinions.
 
I'm really starting to believe that this is from environmental issues.

It has always been an environmental agent causing crohn's disease.

While there is a genetic predisposition, a genetic disease has a static rate of increase amongst the population, crohn's rise is exponential. Something in the environment is causing this disease, you can't get around this anymore.

What's more, the genetic mutations, NOD2 and ATG16L1, point to an intracellular infection.
 
It has always been an environmental agent causing crohn's disease.

While there is a genetic predisposition, a genetic disease has a static rate of increase amongst the population, crohn's rise is exponential. Something in the environment is causing this disease, you can't get around this anymore.

What's more, the genetic mutations, NOD2 and ATG16L1, point to an intracellular infection.

Im assuming this is what you (as well as others) think causes crohns as it hasnt been definately attributed to the any environmental process as far as Im aware
 
as it hasnt been definately attributed to the any environmental process as far as Im aware

No it hasn't, although there's very good candidates that are consistently found in people with CD. AIEC, campylobacter, mycobacteria. Why some people are convinced it's an infectious agent, like I do, is NOD2 and ATG16L1. These mutations leave you extremely vulnerable to specific infections. And since these mutations predispose you to crohn's disease, it's not at all inconceivable that crohn's disease is just a persistent infection causing inflammation, as long as it's not cleared, the inflammation won't die down.

(same is seen in 3rd world countries with untreated TB infections, as long as the infection isn't cleared, they have inflammation, often for years)

I don't think the cause of crohn's disease is an extremely complex interplay between the indigenous flora or a certain Th unbalance. Little kids are getting crohn's disease, immigrants moving to the West get crohn's disease in a matter of months, there's likely a simpler explanation behind the inflammation, such as an infection. As long as the infection isn't cleared, the inflammation will persist, just like with intestinal TB, clinically an extremely similar disease to CD.
 

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