Human noroviruses are the leading cause of acute viral gastroenteritis outbreaks in children and adults every year. High morbidity rates prompt the need for a better understanding of the underlying mechanisms of norovirus disease induction. Excitingly, our lab has recently shown that wildtype neonatal mice are susceptible to diarrheal disease when infected by the murine norovirus strain MNV-1, providing a clinically relevant small animal model to study norovirus disease induction. We therefore used this model to test the hypothesis that MNV-1 encodes an enterotoxin responsible for causing disease. We specifically tested the role of the norovirus minor capsid protein VP2 as an enterotoxin based on its shared structural characteristics with the known rotavirus enterotoxin NSP4. As the genetically related strain MNV-3 is attenuated in its capacity to cause diarrhea despite replicating to comparable levels to MNV-1 in the gut, reciprocal VP2 chimeric viruses were generated and litters of neonatal mice were infected and observed for diarrhea. Our preliminary results suggest that VP2 is not a virulence determinant.