Welsh R M, Burner P A, Holland J J, Oldstone M B, Thompson H A, Villarreal L P
Bull World Health Organ. 1975;52(4-6):403-8.
Lymphocytic choriomeningitis (LCM) virus infection of the mouse is the best-studied model of persistent viral infection. In cell culture, persistent LCM virus infections are associated with the production of large quantities of defective interfering (DI) LCM virus. These defective interfering particles cannot replicate by themselves yet can interfere with the replication of the standard virus and prevent the cytolytic effect caused by the standard virus. It is important to determine the mechanism of interference and to establish whether the DI virus plays a role in vivo. Biological and biochemical properties of the standard and DI virus particles and also virus enzymes are compared. Antigenic analyses reveal that cells releasing only DI virus particles have less cell surface expression of viral antigens than cells releasing the standard virus. In the animal model, the DI virus is shown to have a protective effect against the pathogenesis of the LCM virus disease both in the mouse and in the rat.
小鼠淋巴细胞性脉络丛脑膜炎(LCM)病毒感染是研究最深入的持续性病毒感染模型。在细胞培养中,持续性LCM病毒感染与大量缺陷干扰(DI)LCM病毒的产生有关。这些缺陷干扰颗粒自身不能复制,但能干扰标准病毒的复制并阻止标准病毒引起的细胞溶解作用。确定干扰机制并确定DI病毒在体内是否起作用很重要。比较了标准病毒颗粒和DI病毒颗粒以及病毒酶的生物学和生化特性。抗原分析表明,仅释放DI病毒颗粒的细胞比释放标准病毒的细胞在细胞表面表达的病毒抗原更少。在动物模型中,DI病毒在小鼠和大鼠中均显示出对LCM病毒病发病机制的保护作用。