Rotavirus kills about 0,000 children worldwide, particularly in the developing world. Scientists have long known how the virus takes its toll: It causes the intestine to secrete large amounts of fluid, leading to death from dehydration among vulnerable infants. Now, they understood exactly how the pathogen opens hydrants. In mice, the virus is activated nerves that control the absorption and fluid secretion in the intestine. Despite this knowledge, a drug that could stop the diarrhea is still far.
Several types of infections can cause diarrhea. Toxins released by certain bacteria, including one that leads to cholera and to pathogenic strains Escherichia coli , activate nerves and apparently stimulate the cells of the intestinal mucosa to stimulate water secretion. To see if the rotavirus may also be overstimulating intestinal neurons, Ove Lundgren at the University of Gothenburg in Sweden teamed with Lennart Svensson of the Swedish Institute for Infectious Disease Control in Solna, and several other colleagues.
The researchers applied three types of compounds known to block the neural transmission in the intestine to rotavirus infected mouse intestine kept in solution. The three compounds strongly repressed fluid secretion, reports tomorrow in the team Science . But inhibitors have little effect, if any, on uninfected intestine, indicating that rotavirus was to blame for the excessive neuronal activity. The researchers confirmed these findings with studies in living mice. The "simple" explanation, says Lundgren, is that rotavirus causes the release of chemicals in the intestine that activate the nerve endings in the intestinal mucosa. Nerves activated then turn on the secretory reflexes in cells of the gut lining that chloride ion discharge in the bore of the intestine. This action is designed to draw water into the hole by osmosis.
The discovery is an important step towards the development of a drug against rotavirus diarrhea, said Don Powell of the University of Texas Medical Branch in Galveston. But researchers still do not know the identity of the nerve stimulating substance released during rotavirus infection - information that would be crucial to find drug candidates that block neuronal activity, said Helen Cooke Medical School of Ohio State in Columbus
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