Vitamin A Deficiency Aggravates Rotavirus Infection in CD-1 Mice Through Extensive Involvement of the Gut

Abstract

Rotavirus (RV) is one of the leading causes of life-threatening viral gastroenteritis in infants and animals. More than 100 million children live in endemic areas where they are at risk of rotavirus infection. In the western world, rotavirus is usually a self-limiting disease that involves no major sequelae; however, in the developing world it often leads to morbidity and mortality. One of the major components influencing the prognosis of rotavirus-infected children is their nutritional status. The prevalence of vitamin A deficiency in developing countries, where RV infection can be fatal, encompasses up to 40% of preschool children. We hypothesized, therefore, that vitamin A deficiency in an animal model would aggravate the course of rotavirus disease. CD-1 mice were infected with RV and fed either vitamin A-sufficient or vitamin A-deficient diets. Histological components of the small intestine and colon, stool samples from which rotavirus was recovered, and vitamin A levels were examined. Flattening of the villi along the duodenum was observed in both rotavirus-infected and non-infected vitamin A-deficient mice. Maximal effect was obtained with a combination of vitamin A deficiency and RV infection. The colon of vitamin A-deficient, infected mice displayed a significantly (p < 0.05) smaller glandular area and higher level of mucin, and viral excretion in the stool became significantly (p < 0.01) increased and lasted longer than in controls. We conclude that vitamin A deficiency aggravates the course of RV infection through both small intestinal and colonic damage.