Swine Interferon-Beta (IFN-β) is a type I interferon produced primarily by virus-infected epithelial cells, fibroblasts, macrophages, and dendritic cells in pigs (Sus scrofa domesticus), where it serves as a key early mediator of innate antiviral immunity. Following recognition of viral nucleic acids by pattern recognition receptors such as RIG-I, MDA5, and the cGAS-STING pathway, swine 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 a critical role in host defense against economically significant viral pathogens including porcine reproductive and respiratory syndrome virus (PRRSV), African swine fever virus (ASFV), swine influenza virus, classical swine fever virus (CSFV), and porcine epidemic diarrhea virus (PEDV). Many of these viruses possess mechanisms to suppress or delay IFN-β production, contributing to immune evasion, viral persistence, and disease severity. The timing and magnitude of IFN-β responses influence viral control, inflammation, and vaccine efficacy. In veterinary and translational research, characterization of swine IFN-β supports studies of antiviral immunity, immune evasion strategies, vaccine development, and comparative type I interferon biology in a large-animal model with physiological similarities to humans, enhancing relevance to both animal health and human infectious disease research.