Rabbit Interferon-Beta (IFN-β) is a type I interferon produced primarily by virus-infected epithelial cells, fibroblasts, macrophages, and dendritic cells in rabbits (Oryctolagus cuniculus), where it functions as a key early mediator of innate antiviral immunity. Following recognition of viral nucleic acids by pattern recognition receptors such as RIG-I–like receptors and the cGAS-STING pathway, rabbit IFN-β is rapidly induced and signals through the type I interferon receptor complex (IFNAR1/IFNAR2), activating JAK/STAT signaling and driving expression 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-β plays an important role in host defense against viral pathogens such as rabbit hemorrhagic disease virus (RHDV), myxoma virus, and other emerging rabbit viruses, where the magnitude and timing of interferon responses influence viral control and disease outcome. Viral evasion or dysregulation of IFN-β signaling can contribute to severe systemic disease or persistence. In research settings, rabbits serve as valuable models for viral pathogenesis, poxvirus biology, immunology, and vaccine development, and characterization of rabbit IFN-β supports studies of antiviral mechanisms, host–virus interactions, and comparative type I interferon biology relevant to both veterinary medicine and human infectious disease research.