Gould E A, Buckley A, Groeger B K, Cane P A, Doenhoff M
Arbovirus Research Unit, Winches Farm Field Station, Hertfordshire, U.K.
J Gen Virol. 1987 Dec;68 ( Pt 12):3105-12. doi: 10.1099/0022-1317-68-12-3105.
Enhancement of yellow fever virus neurovirulence for mice by specific antibody was studied with the French neurotropic vaccine strain. Experimental conditions for enhancement required mice between 14 and 40 days old and intraperitoneal administration of a selected monoclonal antibody 24 h before or up to 72 h after intracerebral virus challenge. Virus infectivity titrations were similar in brains of antibody-treated and untreated mice. Virus recovered from brains of mice with enhanced viral infections was neither qualitatively nor quantitatively different from standard virus. Humoral immune responses in enhanced infections were normal, macrophages did not become infected and viraemia was not significant. Both hydrocortisone treatment and complement depletion with cobra venom resulted in prolongation of mouse survival times but virulence enhancement persisted. Antithymocyte serum had no effect on enhancement although it reduced the humoral immune response. It is proposed that virulence enhancement is due to the combined effects of virus-specific antibody on infected cells, complement-mediated cytolysis and resultant host anti-cellular activity. There is no analogy between mechanisms effecting increased arbovirus growth in vitro in the presence of specific antibody and increased yellow fever virus neurovirulence in vivo after parenteral administration of antibody.
使用法国嗜神经疫苗株研究了特异性抗体对小鼠黄热病病毒神经毒力的增强作用。增强作用的实验条件要求小鼠年龄在14至40日龄之间，并在脑内病毒攻击前24小时或攻击后长达72小时腹腔注射选定的单克隆抗体。抗体处理组和未处理组小鼠脑内的病毒感染性滴定结果相似。从病毒感染增强的小鼠脑中回收的病毒在质量和数量上与标准病毒均无差异。增强感染中的体液免疫反应正常，巨噬细胞未被感染，病毒血症不显著。氢化可的松处理和用眼镜蛇毒消耗补体均导致小鼠存活时间延长，但毒力增强持续存在。抗胸腺细胞血清对增强作用无影响，尽管它降低了体液免疫反应。有人提出，毒力增强是由于病毒特异性抗体对感染细胞的联合作用、补体介导的细胞溶解以及由此产生的宿主抗细胞活性。在体外存在特异性抗体时影响虫媒病毒生长增加的机制与经肠胃外给药抗体后体内黄热病病毒神经毒力增加的机制之间没有相似之处。
