Human norovirus is the leading cause of acute gastroenteritis worldwide with 658 million cases and over 200,000 deaths annually. Despite the significance of this pathogen, we have a limited understanding of how noroviruses infect, cause disease and modulate the innate immune response. The programmed cell death pathways are an important part of this innate response to invading pathogens, but little is known about how they contribute to norovirus replication and facilitate clearance and inflammation. In order to asses this we used murine norovirus infection of bone-marrow derived macrophages to look at the pathways activated during infection and determined that along with caspase 3 mediated apoptosis there was evidence of cleaved gasdermin D, a marker of pyroptotic cell death. Furthermore, MNV infections of primary macrophages lacking key components of the cell death pathways were performed to assess the effect on virus growth kinetics. Altered growth kinetics was observed in macrophages missing RIPK1 or expressing a kinase dead mutant. These results provide a new insight into how murine norovirus triggers cell death pathways and host cells control infection.