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将人巨细胞病毒 (HCMV)接种至 8～ 12周龄Balb/c雌雄小鼠腹腔后 ,交配。待雌鼠临产时剖腹取出胎鼠脑双侧大脑皮层 ,进行病毒分离、病理学检测及用地高辛标记的HCMV寡核苷酸探针对大脑皮层细胞压印片进行原位分子杂交检测。病理学研究结果证实 ,鼠脑为侵袭性脑膜脑炎性病理改变 ,并在神经细胞内发现病毒特征性的大的核内嗜碱性包涵体 ;原位杂交结果显示 ,病毒核酸存在于受染神经细胞及神经胶质细胞核内及胞浆内 ;在鼠脑组织上清液中分离出HCMV。且感染组雌鼠血清特异性IgM抗体阳性率为73 9% ,IgG抗体阳性率为 95 7% ;而对照组雌鼠阳性率分别为 4 2 %和 12 5 %。两组间差异高度显著 (P <0 0 1)。感染组雌鼠所生子鼠死胎率及出生后一周内病死率均明显高于正常对照组 (P <0 0 1)。证明 :该病毒能侵袭Balb/c小鼠 ,并通过胎盘感染其子代的中枢神经系统 (CNS)。这种模拟人类HCMV先天性CNS感染的小鼠模型的建立所显示的许多相似的感染和病理过程 ,为进一步研究HCMV先天性CNS感染的病理过程和疫苗的应用提供了可能
Human cytomegalovirus (HCMV) was inoculated into the peritoneal cavity of Balb / c male and female mice aged 8-12 weeks. When the females gave birth, they were removed by cesarean section. The isolated cerebral cortexes were isolated from the fetal rat brains. Virus isolation, pathological examination and HCMV oligonucleotide probes labeled with digoxigenin were used to detect in situ hybridization of cerebral cortex cells. The results of pathology confirmed that the rat brain was an invasive meningoencephalitis pathological change, and found in the nerve cells within the virus characteristic large nuclear basophilic inclusion bodies; in situ hybridization results show that the presence of viral nucleic acid in the infected Nerve cells and glial cells in the nucleus and cytoplasm; isolated from the brain tissue supernatant HCMV. The positive rate of serum specific IgM antibody was 73 9% and the positive rate of IgG antibody was 95 7% in the infected group, while the positive rate in the control group was 42% and 125% respectively. The difference between the two groups was highly significant (P <0.01). The stillbirth rate of the offspring of infected female mice and the mortality within one week after birth were significantly higher than those of the normal control group (P <0.01). Proof: The virus can infect Balb / c mice and infect their offspring’s central nervous system (CNS) with the placenta. The establishment of a mouse model of congenital CNS infection simulating human HCMV shows many similar infection and pathological processes that may provide further evidence for the further study of the pathological processes and vaccine use in HCMV-congenital CNS infection