A chance discovery in mice shows that when mice with a particular Crohn’s gene are exposed to a specific virus, they develop clinical features similar to those in people with Crohn’s Disease. It is the first documentation of genes-environment interaction in Crohn’s, and scientists hope that the discovery is the beginning of many that will further elucidate how genes and environment interact to produce chronic diseases.
The discovery occurred when researchers moved their mouse colony to a superclean facility to keep the animals clean of viruses common in laboratory settings. The researchers had been working with mice that carried a gene called ATG16L1, a risk factor for Crohn’s in people. After the move to the new facility, the mice ceased to exhibit abnormalities in their intestinal cells. The researchers hypothesized that an environmental trigger must be present in one facility and not the other.
The researchers targeted murine norovirus. Norovirus is common in humans–most famously, Norwalk virus. To test whether or not murine norovirus could be the environmental trigger, researchers infected their mice with MNV CR6, a strain of murine norovirus. After 7 days, the mice developed inflammation of the Paneth cells, which was similar to human patients with Crohn’s. Another strain of norovirus did not have the same effect.
The mechanism by which norovirus combines with the particular gene to produce gut abnormalities is unclear. It is also unclear whether the same process is found in humans, which strains of norovirus can induce the abnormalities, and whether other genes are involved.
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| Norwalk Virus |
-Owen Marecic
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