Pang T
Rev Infect Dis. 1983 Mar-Apr;5(2):346-52. doi: 10.1093/clinids/5.2.346.
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.
所提出的假说认为，一种全身性迟发型超敏反应参与了登革出血热/登革休克综合征的发病机制。该假说设想，在单核吞噬细胞表面存在的病毒抗原引发二次感染期间，致敏T淋巴细胞被激活。这些抗原激活的T细胞随后释放多种生物活性化学介质（淋巴因子），进而产生登革出血热/登革休克综合征病例中所见的休克和出血症状。
