Zlotnik I, Peacock S, Grant D P, Batter-Hatton D
Br J Exp Pathol. 1972 Feb;53(1):59-77.
The pathogenesis of the virulent strain of western encephalitis virus was compared with that of the attenuated Clone 15 of the virus. The results of the work showed that the 2 strains replicated equally in the C.N.S. and produced lesions of encephalitis, but whereas in infections with the virulent strain there was 100 per cent mortality, infection with the attenuated strain did not produce signs of disease but gave rise to immunity and protection against challenge with the virulent strain of virus. Differences were also observed in the degree of brain damage and in virus replication curves depending on the route of infection. In Clone 15 the route of infection influenced also the levels of antibody production. Immunosuppression changed the pathological picture of the C.N.S. lesions in that after inoculations with Clone 15, the inflammatory reaction usually prominent in non-immunosuppressed hamsters, was either delayed or partly eliminated, while the degenerative and astrocytic changes became very severe and widespread. At the same time a proportion of immunosuppressed hamsters otherwise resistant succumbed to the infection with the attenuated Clone 15, developed signs of disease and died. Immunosuppressed hamsters infected by the peripheral route with the attenuated strain of virus were not protected against challenge by the i.c. route; on the other hand when such cyclophosphamide treated hamsters were infected with Clone 15 by the i.c. route they became solidly protected against challenge with the virulent strain of W.E.E. virus. After the cessation of the acute lesions of encephalitis, a number of hamsters infected by the attenuated Clone 15 developed subacute or chronic sequelae in the C.N.S., localized in the olfactory cortical regions. These sequelae were found only after i.p., i.d. and respiratory infections but not after i.c. inoculations.
对西部脑炎病毒强毒株的发病机制与该病毒减毒克隆15株的发病机制进行了比较。研究结果表明,这两种毒株在中枢神经系统中的复制情况相同,并产生脑炎病变,但在强毒株感染中死亡率为100%,而减毒株感染未产生疾病体征,但能产生免疫力并抵御强毒株病毒的攻击。根据感染途径的不同,在脑损伤程度和病毒复制曲线方面也观察到了差异。在克隆15株中,感染途径也影响抗体产生水平。免疫抑制改变了中枢神经系统病变的病理表现,即接种克隆15株后,通常在未免疫抑制的仓鼠中明显的炎症反应要么延迟出现,要么部分消除,而变性和星形细胞变化变得非常严重且广泛。与此同时,一部分原本有抵抗力的免疫抑制仓鼠死于减毒克隆15株的感染,出现疾病体征并死亡。经外周途径感染减毒病毒株的免疫抑制仓鼠不能抵御脑内途径的攻击;另一方面,当用环磷酰胺处理的仓鼠经脑内途径感染克隆15株时,它们能牢固地抵御西部脑炎强毒株病毒的攻击。在急性脑炎病变停止后,一些经减毒克隆15株感染的仓鼠在中枢神经系统中出现亚急性或慢性后遗症,局限于嗅皮质区域。这些后遗症仅在腹腔内、皮内和呼吸道感染后出现,而在脑内接种后未出现。