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Synaptic Pathology in Borna Disease Virus Persistent Infection

机译:博尔纳病病毒持续感染的突触病理学

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摘要

Borna disease virus (BDV) infection of newborn rats leads to a persistent infection of the brain, which is associated with behavioral and neuroanatonomical abnormalities. These disorders occur in the absence of lymphoid cell infiltrates, and BDV-induced cell damage is restricted to defined brain areas. To investigate if damage to synaptic structures anteceded neuronal loss in BDV neonatally infected rats, we analyzed at different times postinfection the expression levels of growth-associated protein 43 and synaptophysin, two molecules involved in neuroplasticity processes. We found that BDV induced a progressive and marked decrease in the expression of these synaptic markers, which was followed by a significant loss of cortical neurons. Our findings suggest that BDV persistent infection interferes with neuroplasticity processes in specific cell populations. This, in turn, could affect the proper supply of growth factors and other molecules required for survival of selective neuronal populations within the cortex and limbic system structures.
机译:新生大鼠的博尔纳病病毒(BDV)感染导致大脑的持续感染,这与行为和神经解剖异常有关。这些疾病发生在没有淋巴样细胞浸润的情况下,BDV诱导的细胞损伤仅限于确定的脑区域。为了研究BDV新生鼠的突触结构损伤是否导致神经元丧失,我们在感染后的不同时间分析了生长相关蛋白43和突触素的表达水平,这两个分子参与神经可塑性过程。我们发现BDV诱导这些突触标志​​物的表达进行性和明显的减少,其次是皮质神经元的重大损失。我们的发现表明,BDV持续感染会干扰特定细胞群体中的神经可塑性过程。反过来,这可能会影响皮层和边缘系统结构内选择性神经元群体生存所需的生长因子和其他分子的适当供应。

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