Booss J, Wheelock E F
J Infect Dis. 1977 Mar;135(3):478-81. doi: 10.1093/infdis/135.3.478.
Groups of mice that received a predominantly lethal or a nonlethal dose of murine cytomegalovirus (CMV) were studied prospectively to correlate clinical observations with detection of virus in spleen cells and with the response of spleen cells to the thymus-derived (T-) cell mitogen concanavalin A (con A). In both groups of mice, virus was virtually cleared from spleen cells by day 8 after infection. Depression of the spleen cell response to con A preceded clinical signs of infection, was more severe in the lethally infected group, and improved as clinical signs cleared in the few surviving mice. Serum from infected mice depressed the response of uninfected spleen cells to con A. These findings support the hypothesis that clinical illness and death from CMV infection of mice are a consequence of events that follow the depression of T-cell function by CMV. This depression is at least partially mediated by a humoral mechanism.
对接受主要致死剂量或非致死剂量鼠巨细胞病毒（CMV）的小鼠组进行了前瞻性研究，以将临床观察结果与脾细胞中病毒的检测以及脾细胞对胸腺来源（T）细胞促有丝分裂原刀豆球蛋白A（cona）的反应相关联。在两组小鼠中，感染后第8天病毒几乎从脾细胞中清除。脾细胞对cona反应的抑制先于感染的临床症状，在致死性感染组中更严重，并且随着少数存活小鼠临床症状的消除而改善。感染小鼠的血清抑制了未感染脾细胞对cona的反应。这些发现支持了这样的假设，即小鼠CMV感染引起的临床疾病和死亡是CMV导致T细胞功能抑制后发生的事件的结果。这种抑制至少部分是由体液机制介导的。
