Ferret Interferon-Alpha (IFN-α) is a type I interferon produced primarily by plasmacytoid dendritic cells and virus-infected epithelial and immune cells in ferrets (Mustela putorius furo), where it serves as a critical mediator of early innate antiviral immunity. Upon engagement of the type I interferon receptor complex (IFNAR1/IFNAR2), ferret IFN-α activates the JAK/STAT signaling pathway, leading to induction of interferon-stimulated genes (ISGs) that inhibit viral replication, enhance antigen presentation, and promote activation of natural killer (NK) cells and adaptive immune responses. IFN-α is rapidly upregulated during infection with respiratory viruses such as influenza A virus, SARS-CoV-2, respiratory syncytial virus (RSV), and other emerging pathogens, and its expression levels often correlate with viral load and disease severity. Because ferrets are widely regarded as a gold-standard animal model for human respiratory viral infections and transmission studies, characterization of IFN-α responses is essential for understanding antiviral defense mechanisms, interferon-mediated immunopathology, vaccine efficacy, and antiviral therapeutic development. As both a biomarker and functional regulator of host–virus interactions, ferret IFN-α plays a central role in translational research focused on respiratory disease, immune modulation, and pandemic preparedness.