Myeloid Cell Leukemia-1 knockout leads to increased viral propagation of Respiratory Syncytial Virus and influenza virus in mouse embryonic fibroblast cells and A549 cells: implications in cancer therapy

These findings indicate that Mcl-1 upregulation during RSV and influenza virus infection functions as a critical host antiviral defense mechanism, rather than a viral evasion strategy. Clinically, our results raise concerns regarding therapies that target Mcl-1, such as certain anticancer treatments, which may inadvertently increase susceptibility to severe viral infections. Careful monitoring and potential prophylactic antiviral interventions may be warranted in patients receiving Mcl-1 inhibitor therapies.