Human Interferon-Alpha (IFN-α) is a type I interferon family consisting of multiple closely related subtypes (e.g., IFN-α1, IFN-α2, IFN-α8, IFN-α14, among others) produced primarily by plasmacytoid dendritic cells and virus-infected cells, where it plays a central role in early innate antiviral immunity. Upon binding to the type I interferon receptor complex (IFNAR1/IFNAR2), IFN-α activates the JAK/STAT signaling pathway, leading to induction of hundreds of interferon-stimulated genes (ISGs) that inhibit viral replication, enhance antigen presentation, promote natural killer (NK) cell cytotoxicity, and shape adaptive immune responses. Human IFN-α is critical in defense against viral infections such as influenza, hepatitis B and C viruses, HIV, SARS-CoV-2, and other emerging pathogens, and impaired or delayed IFN-α responses are associated with severe viral disease. Conversely, excessive or chronic IFN-α production contributes to autoimmune and inflammatory disorders including systemic lupus erythematosus (SLE), type I interferonopathies, and certain dermatologic conditions. Clinically, recombinant IFN-α has been used as a therapeutic agent in chronic viral hepatitis and specific malignancies such as hairy cell leukemia and melanoma. As both a biomarker and therapeutic target, human IFN-α is central to research on antiviral immunity, immune dysregulation, cancer immunotherapy, and development of interferon-modulating treatments.