Mitochondria are central regulators of cellular metabolism, bioenergetics, and innate immunity, and are frequent viral targets to promote replication and evade host defenses. This project investigated how influenza A virus (IAV) reprograms mitochondrial dynamics and bioenergetics, and how antiviral responses modulate these processes during infection. We compared two IAV strains: wild-type A/Puerto Rico/8/34 (PR8), with a full-length NS1 protein that suppresses host immunity, and PR8 NS1 N81, a mutant with a truncation at amino acid 81 that impairs immune evasion and enhances MAVS-mediated signaling. This approach allowed us to dissect the contribution of NS1 to mitochondrial remodeling and function. As expected, PR8 induced pronounced mitochondrial fragmentation, whereas NS1 N81 infection preserved normal mitochondrial morphology, resembling non-infected cells. In MAVS-deficient cells, mitochondria were already fragmented even in the absence of infection, suggesting that MAVS helps maintain mitochondrial integrity and that changes in morphology may precede innate immune activation. Bioenergetic profiling revealed that both PR8 and, to a lesser extent, NS1 N81 reduced proton leak at late stages of infection, accompanied by decreased UCP2 mRNA levels. PR8 also decreased complex I activity while increasing complex V ATPase activity, suggesting enhanced ATP consumption. These alterations were not observed for NS1 N81, indicating differential control of mitochondrial energy metabolism. Overall, our findings suggest that IAV modulated mitochondrial dynamics and bioenergetic functions in distinct manners depending on the viral protein NS1. We hypothesized that cells sense IAV-induced stress, leading to mitochondrial fragmentation and alterations in bioenergetics that are restored once innate immunity is activated.