Human noroviruses are the leading cause of acute gastroenteritis outbreaks in children and adults every year. Over 685 million cases of norovirus infection were estimated to occur last year. This high incidence of morbidity prompts the need for a better understanding of the underlying pathogenic mechanisms of norovirus disease induction. Excitingly, our lab has recently show that wild type neonatal mice are susceptible to symptoms of diarrhea and weight loss when infected by MNV-1, an acute murine norovirus strain. The goal of my project is to use this neonatal mouse model to test whether MNV-1 encodes a protein that acts as an enterotoxin. We hypothesize that the MNV-1 VP2 protein, a structural protein on the interior of the viral capsid, is an enterotoxin. Our previous studies have revealed that the MNV-1 strain causes diarrhea, weight loss, and intestinal fluid accumulation in BALB/c neonatal mice whereas the genetically related MNV-3 strain is attenuated in the same model. Using these differences, I will generate chimeric viruses in which the gene encoding VP2 from each parental virus is replaced with the VP2-encoding gene from the other virus. Litters of neonatal BALB/c mice will be infected, and gastroenteritis symptoms will be measured and compared.