Abstract
Rotavirus is responsible for infantile gastroenteritis and each year causes 440 000 deaths worldwide. The virus infects the mature enterocytes of the villus tip of the small intestine and induces a watery diarrhea. Diarrhea can occur with no visible tissue damage and, conversely, the histological lesions can be asymptomatic. Rotavirus infection impairs intestinal disaccharidases and Na+-solute symports coupled to water transport. Maldigestion of carbohydrates and their accumulation in the intestinal lumen as well as malabsorption of nutriments and a concomitant inhibition of water reabsorption would lead to osmotic diarrhea. The hypothesis that the NSP4 viral enterotoxin, by mobilizing intracellular calcium, would be a secretory agonist remains to be demonstrated. In rotavirus diarrhea, Cl- reabsorption in villi is stimulated and secretion in crypt is unaffected, questioning the origin of Cl- secreted into the intestinal lumen, which possibly arises from the villus base cells. These mechanisms appear to be quite different from those used by bacterial enterotoxins that cause "pure" secretory diarrhea. The viral enterotoxin would induce mainly osmotic diarrhea, especially since NSP4 has been shown to be directly responsible for glucosegalactose malabsorption.
Published Version
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