Caprine Interferon-Alpha (IFN-α) is a type I interferon produced primarily by plasmacytoid dendritic cells and virus-infected cells in goats (Capra hircus), where it plays a central role in early innate antiviral immunity. Upon binding to the type I interferon receptor complex (IFNAR1/IFNAR2), caprine 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. In caprine health, IFN-α is critically involved in host defense against economically significant viral infections such as caprine arthritis encephalitis virus (CAEV), peste des petits ruminants virus (PPRV), goatpox virus, bluetongue virus, and other small ruminant pathogens. Impaired or evaded type I interferon responses can contribute to viral persistence and chronic inflammatory disease. As both a biomarker and functional mediator of antiviral immunity, caprine IFN-α is important for vaccine evaluation, antiviral strategy development, and studies of host–virus interactions. In comparative and translational research, characterization of caprine IFN-α supports investigations into lentiviral pathogenesis (CAEV as a model for small ruminant lentivirus infections), mucosal antiviral immunity, and type I interferon biology relevant to both veterinary medicine and broader immunological research.