The interaction of vitamin A deficiency and rotavirus infection

Abstract

We have established an experimental model of vitamin A deficiency in the mouse. Animals fed an appropriate diet showed greatly reduced circulating vitamin A levels and depleted liver vitamin A stores after 12 weeks. Rotavirus infection produced marked histopathological changes in the gut of deficient mice when compared with normal and pairfed controls. The spleen weight was increased in deficient infected animals which also showed altered rotavirus antibody levels measured by the ELISA technique. Goblet cell number in the villi was reduced in vitamin A deficient animals and this may have contributed to the susceptibility of adult deficient mice to rotavirus infection. Cell mediated immunity, measured as the delayed type hypersensitivity response to picryl chloride was reduced in animals with vitamin A deficiency. In parallel studies the effect of a reduction in total food intake was measured in mice receiving up to 50% less diet for 7 or 12 weeks. Although some histological abnormalities were detected in the gut of the animals grossly deficient in the diet, rotavirus infection did not produce intestinal damage beyond this. Delayed hypersensitivity and anti rotavirus antibody levels following oral challenge were normal in animals on a reduced intake.

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