The hypothesis presented proposes the involvement of a systemic form of a delayed-type hypersensitivity reaction in the pathogenesis of dengue hemorrhagic fever/dengue shock syndrome. It envisages the activation of sensitized T lymphocytes during a secondary infection by viral antigen present on the surfaces of mononuclear phagocytic cells. These antigen-activated T cells then release a variety of biologically active chemical mediators (lymphokines), which then produce the symptoms of shock and hemorrhage seen in cases of dengue hemorrhagic fever/dengue shock syndrome.