Volkert M, Bro-Jorgensen K, Marker O
Bull World Health Organ. 1975;52(4-6):471-8.
The initiation of persistent infections with the Traub strain of the LCM virus is dependent not only on the number of immunocompetent cells present in the infected animals but probably also on the fact that the virus depresses the development of the bone marrow cells and causes a pronounced immunosuppression at the T cell level. By analysing the events leading to the termination of the virus carrier state by adoptive immunization, it was clearly demonstrated that the cellular immunity provoked was solely responsible for the virus elimination. Furthermore, helper T cells were shown to be necessary for the production of antibodies, which also occurs in adoptively immunized mice. In view of this finding, further experiments were performed, which strongly indicated that neither LCM-primed B cells nor LCM-primed helper T cells are present in mice that are persistent virus carriers. Similarly, neither cellular immunity to the LCM virus nor the presence of enhancing factors or suppressor cells could be detected. It is concluded that C(3)H mice that are persistent virus carriers have developed a humoral as well as a cellular immunological tolerance to the LCM virus.
淋巴细胞性脉络丛脑膜炎病毒（LCM病毒）特劳伯毒株持续感染的引发不仅取决于受感染动物体内免疫活性细胞的数量，还可能取决于该病毒抑制骨髓细胞发育并在T细胞水平引起明显免疫抑制这一事实。通过分析过继免疫导致病毒携带状态终止的过程，清楚地表明所激发的细胞免疫是病毒清除的唯一原因。此外，辅助性T细胞被证明是产生抗体所必需的，这在过继免疫的小鼠中也会发生。鉴于这一发现，进行了进一步的实验，这些实验有力地表明，持续病毒携带者小鼠体内既不存在LCM致敏的B细胞，也不存在LCM致敏的辅助性T细胞。同样，既检测不到对LCM病毒的细胞免疫，也检测不到增强因子或抑制细胞的存在。得出的结论是，持续病毒携带者的C(3)H小鼠已对LCM病毒产生了体液免疫和细胞免疫耐受。
