Weiland F, Cox J H, Meyer S, Dahme E, Reddehase M J
Federal Research Centre for Virus Diseases of Animals, Tübingen, Germany.
J Virol. 1992 Aug;66(8):5096-9. doi: 10.1128/JVI.66.8.5096-5099.1992.
Two pathogenetically distinct disease manifestations are distinguished in a murine model of primary rabies virus infection with the Evelyn-Rokitnicky-Abelseth strain, rabies virus neuritic paralysis (RVNP) and fatal encephalopathogenic rabies. RVNP develops with high incidence in immunocompetent mice after intraplantar infection as a flaccid paralysis restricted to the infected limb. The histopathologic correlate of this monoplegia is a degeneration of the myelinated motor neurons of the peripheral nerve involved. While, in this model, fatal encephalopathogenic rabies develops only after depletion of the CD4 subset of T lymphocytes and without contribution of the CD8 subset, RVNP is identified as an immunopathological process in which both the CD4 and CD8 subsets of T lymphocytes are critically implicated.
在用伊夫林-罗基特尼茨基-阿贝尔塞斯毒株进行原发性狂犬病病毒感染的小鼠模型中，可区分出两种病因截然不同的疾病表现，即狂犬病病毒神经麻痹（RVNP）和致命性脑型狂犬病。在免疫功能正常的小鼠中，经足底感染后，RVNP的发病率很高，表现为局限于感染肢体的弛缓性麻痹。这种单瘫的组织病理学相关表现是受累外周神经有髓运动神经元的变性。而在该模型中，致命性脑型狂犬病仅在T淋巴细胞的CD4亚群耗竭后发生，且CD8亚群无作用，RVNP则被确定为一种免疫病理过程，其中T淋巴细胞的CD4和CD8亚群都至关重要。
