Hirsch R L, Griffin D E, Winkelstein J A
J Immunol. 1978 Oct;121(4):1276-8.
The course of Sindbis virus infection in 12-day-old BALB/c mice was altered significantly in animals depleted of the third component of complement (C3) by treatment with purified cobra venom factor (CoVF). Although the same percentage of C3-depleted and normal animals died (30%) after the subcutaneous inoculation of 1000 PFU Sindbis virus, the mean day of death was later in C3-depleted mice (8.4 days) than in controls (6.5 days). In addition, morbidity was prolonged in C3-depleted mice. Growth of virus at the inoculation site in the foot was not different; however, viremia was prolonged and the amount of virus in the brain was 1000-fold greater 6 days after infection in C3-depleted animals. These studies demonstrated that complement plays an important role in the host's response to Sindbis virus infection by participating in both beneficial and immunopathologic responses to the infection.
通过用纯化的眼镜蛇毒因子(CoVF)处理,使12日龄BALB/c小鼠体内补体第三成分(C3)缺失,这显著改变了辛德毕斯病毒在这些小鼠中的感染进程。尽管皮下接种1000个空斑形成单位(PFU)辛德毕斯病毒后,C3缺失小鼠和正常小鼠的死亡百分比相同(均为30%),但C3缺失小鼠的平均死亡天数(8.4天)比对照组(6.5天)更晚。此外,C3缺失小鼠的发病期延长。病毒在足部接种部位的生长情况并无差异;然而,病毒血症持续时间延长,且在感染6天后,C3缺失动物脑内的病毒量比正常动物高1000倍。这些研究表明,补体通过参与对感染的有益反应和免疫病理反应,在宿主对辛德毕斯病毒感染的应答中发挥重要作用。