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首页> 外文期刊>Neuropathology and applied neurobiology >Distemper virus encephalitis exerts detrimental effects on hippocampal neurogenesis
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Distemper virus encephalitis exerts detrimental effects on hippocampal neurogenesis

机译：瘟热病毒脑炎对海马神经发生有不利影响

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Aims: Despite knowledge about the impact of brain inflammation on hippocampal neurogenesis, data on the influence of virus encephalitis on dentate granule cell neurogenesis are so far limited. Canine distemper is considered an interesting model of virus encephalitis, which can be associated with a chronic progressing disease course and can cause symptomatic seizures. Methods: To determine the impact of canine distemper virus (CDV) infection on hippocampal neurogenesis, we compared post-mortem tissue from dogs with infection with and without seizures, from epileptic dogs with non-viral aetiology and from dogs without central nervous system diseases. Results: The majority of animals with infection and with epilepsy of non-viral aetiology exhibited neuronal progenitor numbers below the age average in controls. Virus infection with and without seizures significantly decreased the mean number of neuronal progenitor cells by 43% and 76% as compared to age-matched controls. Ki-67 labelling demonstrated that hippocampal cell proliferation was neither affected by infection nor by epilepsy of non-viral aetiology. Analysis of CDV infection in cells expressing caspase-3, doublecortin or Ki-67 indicated that infection of neuronal progenitor cells is extremely rare and suggests that infection might damage non-differentiated progenitor cells, hamper neuronal differentiation and promote glial differentiation. A high inter-individual variance in the number of lectin-reactive microglial cells was evident in dogs with distemper infection. Statistical analyses did not reveal a correlation between the number of lectin-reactive microglia cells and neuronal progenitor cells. Conclusions: Our data demonstrate that virus encephalitis with and without seizures can exert detrimental effects on hippocampal neurogenesis, which might contribute to long-term consequences of the disease. The lack of a significant impact of distemper virus on Ki-67-labelled cells indicates that the infection affected neuronal differentiation and survival of newborn cells rather than hippocampal cell proliferation.
机译：目的：尽管了解脑炎症对海马神经发生的影响，但有关病毒性脑炎对齿状颗粒细胞神经发生影响的数据仍然有限。犬瘟热被认为是病毒性脑炎的一种有趣模型，它可能与疾病的慢性发展有关，并可能导致症状性癫痫发作。方法：为了确定犬瘟热病毒（CDV）感染对海马神经发生的影响，我们比较了有无癫痫发作的犬，无病毒病因的癫痫犬和无中枢神经系统疾病的犬的死后组织。结果：大多数感染并患有非病毒性病因癫痫病的动物的神经元祖细胞数量均低于对照组的平均年龄。与年龄匹配的对照组相比，有或无癫痫发作的病毒感染均使神经元祖细胞的平均数量显着降低了43％和76％。 Ki-67标记表明海马细胞增殖既不受感染也不受非病毒病因癫痫的影响。对表达caspase-3，doublecortin或Ki-67的细胞中CDV感染的分析表明，神经元祖细胞的感染极为罕见，这表明感染可能会损害未分化的祖细胞，阻碍神经元分化并促进神经胶质分化。在患犬瘟热的狗中，凝集素反应性小胶质细胞数量的个体差异很大。统计分析未显示凝集素反应性小胶质细胞与神经元祖细胞数量之间的相关性。结论：我们的数据表明，伴有或不伴有癫痫发作的病毒性脑炎可能会对海马神经发生产生有害影响，这可能会导致疾病的长期后果。瘟热病毒对Ki-67标记的细胞缺乏显着影响，表明该感染影响新生细胞的神经元分化和存活，而不是海马细胞增殖。

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