GENETICALLY CONTROLLED MECHANISMS OF RECOVERY FROM FRIEND VIRUS-INDUCED LEUKEMIA

这个项目的目标是了解宿主防御和 对逆转录病毒的免疫力。以前的工作已经定义了几个鼠标 影响小鼠自愈能力的基因 病毒复合体(FV)诱导的白血病。其中一些基因也会影响 通过接种疫苗来诱导对这种疾病的保护性免疫的能力 佐剂中的病毒蛋白或在重组痘苗病毒中表达。 最新的研究表明，保护性免疫可以通过 逆转录病毒囊膜蛋白和Gag蛋白均在牛痘中表达。删除 GAG多肽的氨基或羧基末端的比对表明 氨基末端的一半负责免疫保护。这 保护作用弱于病毒包膜蛋白诱导的保护，但 它在小鼠身上成功了，这些小鼠不能成功地 对包膜蛋白的免疫反应。这些结果表明， 包膜蛋白和GAG蛋白应被视为可能的免疫原 构建针对其他逆转录病毒的疫苗。它的作用机制 GAG蛋白免疫的保护作用正在进一步研究中。

The goal of this project is to understand mechanisms of host defense and immunity against retroviruses. Previous work has defined several mouse genes which influence ability of mice to recover spontaneously from Friend virus complex (FV)-induced leukemia. Some of these genes also influence ability to induce protective immunity to this disease by vaccination with viral protein in adjuvants or expressed in recombinant vaccinia viruses. The most recent work has shown that protective immunity can be induced by both retroviral envelope and gag proteins expressed in vaccinia. Deletion of the amino or carboxy-termini of the gag polyprotein indicated that the amino-terminal half was responsible for the immune protection. This protection was weaker than that induced by the viral envelope protein, but it was successful in mice who were not capable of making a successful immune response to the envelope protein. These results suggested that both envelope and gag proteins should be considered as possible immunogens in constructing vaccines against other retroviruses. The mechanism of protection by immunization with gag protein is under further investigation.