Howell D M, Martz E
Department of Microbiology, University of Massachusetts, Amherst 01003.
J Gen Virol. 1987 Nov;68 ( Pt 11):2899-907. doi: 10.1099/0022-1317-68-11-2899.
Cytotoxic T lymphocytes (CTLs) induce rapid, extensive internal disintegration in target cells and this is unique among immune lytic mechanisms studied. This raises the question of whether CTLs are uniquely capable of halting virus infections by inducing damage within the target cell causing inactivation of intracellular virus. Reovirus infection of mouse P815 cells provided a suitable system for evaluating this question. An increase in cell-associated infectious virions began 8 h after infection and increased until 20 h post-infection, at which time the titre levelled off at about 100- to 1000-fold higher than the initial value. The infectious activity was compared between host cells killed by CTLs and those killed by sonication at various points in the infection cycle. The presence of reovirus within the target cell did not inhibit the usual internal disintegration events associated with the death of a target killed by CTLs. Nevertheless, the results indicated that CTLs were incapable of inactivating intracellular reovirus at any point in the life cycle of the virus: CTL-induced cytolysis simply released the infectious virions into the medium. Thus, at least in the case of reovirus, the utility of direct killing by CTLs would appear to be limited to reduction of the virus yield by lysis of the host cell before virus replication and assembly is completed.
细胞毒性T淋巴细胞（CTLs）可诱导靶细胞迅速发生广泛的内部崩解，这在已研究的免疫溶解机制中是独一无二的。这就提出了一个问题，即CTLs是否具有独特的能力，通过在靶细胞内诱导损伤从而使细胞内病毒失活，来阻止病毒感染。呼肠孤病毒感染小鼠P815细胞为评估这个问题提供了一个合适的系统。感染后8小时，细胞相关感染性病毒粒子开始增加，并持续增加直至感染后20小时，此时滴度趋于稳定，比初始值高约100至1000倍。在感染周期的不同时间点，比较了被CTLs杀死的宿主细胞和被超声处理杀死的宿主细胞之间的感染活性。靶细胞内呼肠孤病毒的存在并不抑制与被CTLs杀死的靶细胞死亡相关的常见内部崩解事件。然而，结果表明，CTLs在病毒生命周期的任何阶段都无法使细胞内呼肠孤病毒失活：CTLs诱导的细胞溶解只是将感染性病毒粒子释放到培养基中。因此，至少就呼肠孤病毒而言，CTLs直接杀伤的作用似乎仅限于在病毒复制和组装完成之前通过裂解宿主细胞来降低病毒产量。
