MAVS and infection: Using fluorescent in situ hybridization targeting ribonucleic acid molecules (RNA FISH) to distinguish DVGs from standard viral genomes during infection, we reveal that during infection with the murine parainfluenza virus Sendai (SeV) or RSV DVGs accumulate only in a subpopulation of infected cells, and that these cells survive the infection longer than cells enriched in full-length virus Survival of DVG-high cells is dependent on MAVS signaling, and we identify TNFα produced in response to MAVS signaling as pivotal in determining cell fate during SeV infection.