There's also a
New York Times article.
So, this research could potentially have implications for people with IBS.
The title of the science articles are unhelpful: There are conflicting findings, depending on the genes of the mice. The importance of the findings are based upon the idea that the virus can be beneficial
or harmful, depending on the genes of the infected individual. And this may have implications for people with inflammatory bowel disease.
I struggled to follow the logic of the articles, but my understanding so far is that...
Germ Free Mice
Germ-free mice fail to develop a mature gut, including failing to produce adequate villi, and failing to mount a proper gut immune response.
"Germ-free mice also fail to develop a normal supply of the immune cells nestled in the lining of the gut, which attack pathogens but not harmless microbes. As a result, the germ-free mouse’s gut becomes vulnerable to injuries and infections."
However, when germ-free mice were administered murine norovirus (which is harmless in healthy mice - and is related to the human strain that causes vomiting and diarrhoea) "the animals developed intestines and an immune system that were fairly normal."
Mice bred with mutation
Now, we switch the discussion from germ-free mice, to mice bred with a genetic mutation which is known to increase the risk of inflammatory bowel disease in humans. When these mutated mice are exposed to murine norovirus (harmless in healthy mice), they develop gut inflammation or "inflammatory bowel disease."
Normal Adult Mice
When normal adult mice were administered with antibiotics, the guts returned to normal when the antibiotics were followed by administering the murine norovirus. Also, normal mice that were exposed to gut damage, survived longer if they were pre-exposed to the murine norovirus.
Humans
When taking antibiotics, our villi are damaged.
"Heavy doses of antibiotics, which kill off much of the microbiome, can lead to drastic changes in the gut. Some villi die, and the population of immune cells drops. But as bacteria return to the gut, the damage gets fixed."
My Conclusion
So, if I've understood it correctly, normal and germ-free mice benefit from infection with the virus, but mice genetically predisposed to inflammatory bowel disorder (because of a genetic mutation) developed inflammatory bowel disease.
"When [the researchers] prevented germ-free mice from making a [specific] receptor on the surface of their cells, infection with norovirus didn’t lead to an improvement in their guts. That receptor only latches onto one type of molecule. It’s called
Type 1 interferon, and it’s produced by cells when they’re invaded by viruses."
So perhaps there's a therapeutic clue there, for people with IBD?
Sounds like it could have interesting potential implications for people with IBS.