Abstract
Infection of host cells by mammalian reovirus in culture or in tissues of infected animals results in cell death. Cell death of infected neurons and myocytes contributes to the pathogenesis of reovirus-induced encephalitis and myocarditis in a newborn mouse model. Thus, reovirus-induced cell death has been used to investigate the basis of viral disease. Depending on the cell type, infection of host cells by reovirus results in one of two forms of cell death-apoptosis and necroptosis. In addition to the obvious differences in how these two forms of cell death are executed, the mechanisms by which reovirus infection initiates and transduces signals that lead to each of these types of cell death are distinct. In this review, we discuss how apoptosis and necroptosis are triggered by events at different stages of infection. We also describe how innate immune recognition of reovirus genomic material and type I interferon signaling pathways connect with the core components of the apoptosis and necroptosis machinery. The impact of different cell death mediators on viral pathogenesis and the potential of reovirus as an oncolytic vector are also outlined.