Jubelt B, Narayan O, Johnson R T
J Neuropathol Exp Neurol. 1980 Mar;39(2):149-59. doi: 10.1097/00005072-198003000-00004.
The mechanism of resistance of newborn mice to poliovirus-induced paralysis was studied by comparing regional virus replication in the adult and in the newborn central nervous systems (CNS) after intracerebral (ic) and intraspinal inoculation. Initial virus replication in the brains was similar in both age groups. Paralysis correlated with replication of virus in the spinal cord to a constant threshold, and this replication in newborns was delayed. Intraspinal inoculation of newborns eliminated the delay, indicating that neonatal anterior horn motor neurons were fully susceptible to infection. Cordectomy prevented the spread of virus, despite patent cerebrospinal fluid (CSF) pathways. Thus, poliovirus appeared to spread within the CNS via an axonal transport system. Known maturational changes in the fast transport system may explain the relative resistance of immature mice to poliovirus-induced paralysis.
通过比较脑内(ic)和脊髓内接种后成年和新生小鼠中枢神经系统(CNS)中局部病毒复制情况,研究了新生小鼠对脊髓灰质炎病毒诱导麻痹的抵抗机制。两个年龄组脑内最初的病毒复制情况相似。麻痹与脊髓中病毒复制达到恒定阈值相关,新生小鼠的这种复制延迟。对新生小鼠进行脊髓内接种消除了延迟,表明新生的前角运动神经元对感染完全敏感。尽管脑脊液(CSF)通路畅通,但脊髓切除术阻止了病毒传播。因此,脊髓灰质炎病毒似乎通过轴突运输系统在中枢神经系统内传播。快速运输系统中已知的成熟变化可能解释了未成熟小鼠对脊髓灰质炎病毒诱导麻痹的相对抵抗力。