Oncolytic reovirus demonstrates mixed results in clinical trials. To achieve better clinical outcomes a more complete understanding of reovirus infection is needed. Efficient reovirus infection often culminates in cell death by apoptosis. Mitochondria play essential roles regulating apoptosis and oxidative phosphorylation. Although mitochondria are implicated in integrating reovirus-induced apoptotic signaling, no study has explored how modulating apoptotic pathways or mitochondrial metabolism influences reovirus infection.
I demonstrate that directly priming apoptotic pathways may be an effective strategy for augmenting reovirus-induced cytolysis in pediatric leukemia cells and possibly other cancer cells. Further study is warranted to explore the clinical potential of this strategy. The experiments attempting to modulate mitochondrial function may be consistent with a role for mitochondrial respiration in reovirus infection. However, the influence of mitochondrial metabolism on reovirus infection requires more directed study in the future.