Equine Interferon-Beta (IFN-β) is a type I interferon produced primarily by virus-infected epithelial cells, fibroblasts, macrophages, and dendritic cells in horses (Equus caballus), 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–like receptors and the cGAS-STING pathway, equine IFN-β is rapidly induced and signals through the type I interferon receptor complex (IFNAR1/IFNAR2), activating JAK/STAT signaling and promoting expression of interferon-stimulated genes (ISGs) that suppress viral replication, enhance antigen presentation, and stimulate natural killer (NK) cell and adaptive immune responses. IFN-β is critically involved in host defense against important equine viral pathogens including equine influenza virus, equine herpesvirus-1 and -4 (EHV-1/EHV-4), West Nile virus, and equine arteritis virus, and the timing and magnitude of IFN-β production can influence viral control, inflammation, and clinical outcome. Viral evasion or dysregulation of IFN-β signaling may contribute to persistent infection or immunopathology. In veterinary and translational research, characterization of equine IFN-β supports studies of respiratory and neurotropic viral pathogenesis, antiviral therapeutics, vaccine development, and comparative type I interferon biology in large-animal models relevant to both equine and human infectious disease research.