The influences of dietary deficiencies of folic acid or zinc on rotaviral disease infant mice were studied. Preliminary studies indicated that bovine and simian rotaviruses, but not porcine rotavirus, caused diarrhea in infant mice. Bovine and porcine rotaviruses were not, however, sufficiently infectious to replace murine rotavirus in studies utilizing the murine model. It was also determined that murine rotavirus purified by a cesium chloride gradient was highly infectious and useful for subsequent studies on nutritional influences of rotaviral disease. In dietary studies, female Swiss Webster mice were fed diets containing deficient, moderately deficient, or adequate levels of folic acid or zinc. The quantity of s[specific nutrient added to the tow diets were 0, 0.125, and 0.50 ug of folic acid per gram of diet, and 4, 12, and 60 ug of zinc per gram of diet. The infants from these mice were orally inoculated with approximately 100 ID of purified murine rotavirus with sterile diluent as a control. Uninfected infants from dams fed the lowest folic acid diet gained weight at a significantly reduced rate compared with the two groups fed the higher dietary folic acid levels. Infants from the same low folic acid group had significantly less folate levels in their livers which indicated that a deficiency was achieved. A moderate enhancement of rotaviral disease was seen in these folic acid-deprived infants as determined by their decreased ability to gain weight, increased incidences of diarrhea, and an increased number which exhibited high rotaviral antigen titers in their intestines. Serum rotaviral antibody titers were below detectable levels in a significant number of animals fed the lowest folic acid diet. Zinc deficiency in the infant mice was evidenced by significantly reduced thymus weight, inability to gain body weight, lower zinc concentration in whole infant mice, alopecia and presence of skin rashes. The zinc deficiency produced in this study did not significantly affect weight gained by the infants, presence of diarrhea, titers of virus recovered from the intestine, rotaviral specific antibody in sera, rotaviral specific antibody in milk, ratio of intestine wieght to whole mouse weight, and serum sodium levels. Since zinc deficiency did not alter the rotaviral diesease, studies with athymic nude mice were done. After per os rotaviral exposure none of the athymic mice, while all of the mice with thumuses, had serum antibodies specific to rotavirus, demonstrating that elicitation of rotaviral specific antibodies was T-cell dependent.