Zschiesche W, Veckenstedt A
Exp Pathol (Jena). 1979;17(7-8):387-93. doi: 10.1016/s0014-4908(79)80056-3.
Mengo virus has been described to cause, in dependence on the virus dose, lethal panencephalomyelitis and exocrine pancreatitis in mice after i.p. inoculation. Two immunosuppressive agents, cyclophosphamide and 1,3-bis(piperidinomethyl)-5-ethyl-5-phenyl-barbituric acid (ZIMET 176/68), were shown to potentiate Mengo virus infection as demonstrated by histopathology and enhanced mortality. Organotropism of Mengo virus did not change under the drug treatment. However, the histological lesions in brain, spinal cord and pancreas failed to exhibit any inflammatory reaction in case of cyclophosphamide, due to its antiphlogistic properties. Considering the mode of action of the drugs employed and the pathogenesis of Mengo virus infection in mice, it is concluded that in the system used both cyclophosphamide and ZIMET 176/68 exert their potentiating effects by interfering with primary virus-macrophage interaction.
据描述，将门戈病毒经腹腔接种到小鼠体内后，根据病毒剂量的不同，可导致小鼠发生致死性全脑脊髓炎和外分泌性胰腺炎。两种免疫抑制剂，即环磷酰胺和1,3 - 双（哌啶甲基）-5 - 乙基 - 5 - 苯基巴比妥酸（ZIMET 176/68），经组织病理学检查和死亡率增加证实，它们可增强门戈病毒感染。在药物治疗下，门戈病毒的嗜器官性并未改变。然而，由于环磷酰胺具有抗炎特性，其治疗后，脑、脊髓和胰腺的组织学病变未表现出任何炎症反应。考虑到所用药物的作用方式以及小鼠门戈病毒感染的发病机制，得出的结论是，在所用系统中，环磷酰胺和ZIMET 176/68均通过干扰病毒与巨噬细胞的初始相互作用发挥其增强作用。
