Auwaerter P G, Kaneshima H, McCune J M, Wiegand G, Griffin D E
Department of Medicine, John Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
J Virol. 1996 Jun;70(6):3734-40. doi: 10.1128/JVI.70.6.3734-3740.1996.
Mortality from measles is caused mostly by secondary infections associated with the depression of cellular immunity. The mechanism of immune suppression and the role of virus strain differences on the immune system are incompletely understood. SCID-hu mice were used to determine the effects of virulent, wild-type (Chicago-1) and avirulent, vaccine (Moraten) strains of measles virus (MV) on the human thymus in vivo. Chicago-1 replicated rapidly, with a 100-fold decrease in numbers of thymocytes, whereas Moraten replicated slowly, without significant thymocyte death. Productive MV infection occurred not in thymocytes but in thymic epithelial and myelomonocytic cells. Wild-type MV infection of thymic stromata leads to induction of thymocyte apoptosis and may contribute to a long-term alteration of immune responses. The extent of thymic disruption reflects the virulence of the virus, and therefore the SCID-hu mouse may serve as the first small animal model for the study of MV pathogenesis.
麻疹致死主要是由与细胞免疫抑制相关的继发感染所致。免疫抑制机制以及病毒株差异对免疫系统的作用尚未完全明确。利用重症联合免疫缺陷-人（SCID-hu）小鼠来确定麻疹病毒（MV）的强毒株、野生型（芝加哥-1株）和无毒株、疫苗株（莫拉坦株）在体内对人胸腺的影响。芝加哥-1株迅速复制，胸腺细胞数量减少100倍，而莫拉坦株复制缓慢，未出现明显的胸腺细胞死亡。有活性的MV感染并非发生在胸腺细胞中，而是发生在胸腺上皮细胞和骨髓单核细胞中。胸腺基质的野生型MV感染会导致胸腺细胞凋亡，并可能导致免疫反应的长期改变。胸腺破坏的程度反映了病毒的毒力，因此SCID-hu小鼠可作为首个用于研究MV发病机制的小动物模型。
