Hilmas D E, Whitmire R E, Dill G S
Am J Vet Res. 1977 Sep;38(9):1413-9.
A highly virulent strain of Venezuelan equine encephalomyelitis (VEE) virus produced less severe histopathologic changes in brain tissues of mice previously exposed to sublethal total-body x-irradiation than it caused in nonirradiated mice. Prior exposure to 600 R of x-irradiation virtually eliminated the lesions of vasculitis and encephalitis that were found in the infected nonirradiated control mice. Mean peak brain lesion scores generally decreased as radiation exposure dose was increased. Irradiation of mice before inoculation often decreased median time to death, whereas the severity of pathologic changes in brain tissues from inoculated irradiated mice was often reduced, without significantly altering ultimate host survival. The inflammatory response did not appear to have a significant role in clearance of this virus from the brain. There was no evidence that participation of the immune response contributed to total mortality from VEE virus encephalitis, as indicated by the failure of radiation immunosuppression to reduce mortality. Death apparently was caused by the direct cytocidal effects of VEE virus replication.
一种高毒力的委内瑞拉马脑炎（VEE）病毒株，在先前接受亚致死全身X射线照射的小鼠脑组织中引起的组织病理学变化，比在未受照射的小鼠中引起的变化要轻。预先接受600伦琴的X射线照射，实际上消除了在受感染的未照射对照小鼠中发现的血管炎和脑炎病变。随着辐射暴露剂量的增加，平均脑损伤峰值评分通常会降低。在接种前对小鼠进行照射，通常会缩短中位死亡时间，而接种后受照射小鼠脑组织中的病理变化严重程度通常会降低，而不会显著改变最终宿主的存活率。炎症反应似乎在该病毒从脑中清除的过程中没有显著作用。没有证据表明免疫反应的参与导致了VEE病毒脑炎的总死亡率，这一点从辐射免疫抑制未能降低死亡率可以看出。死亡显然是由VEE病毒复制的直接杀细胞作用引起的。
