ROLE OF ENDOGENOUS AND RECOMBINANT RETROVIRUSES IN LEUKEMIA AND DIFFERENTIATION

本项目的主要目的是研究 逆转录病毒诱导的致病机制。我们一直在研究贫血 新生小鼠接种卡介苗诱发的红白血病 Friend鼠白血病辅助病毒(F-MuLV)。这种病有 两个不同的致病阶段都会导致贫血和 脾肿大。红系病毒感染的第一阶段 前体会导致红细胞过早破坏，从而导致 溶血性贫血；代偿性脾肿大 红血球生成。第二期由红白血病组成。 脾肿大和贫血是由于缺乏生产和 红细胞分化。使用两种不同的病毒变体 在毒力方面，表明病毒包膜基因是 早期严重溶血的主要诱因 贫血，而病毒LTR区域对 红白血病感染潜伏期。目前的努力是 旨在确定与基因序列有关的精确基因 这些影响中的每一种。

The main objective of this project is study of mechanisms of retrovirus-induced pathogenesis. We have been studying anemia and erythroleukemia induced by neonatal inoculation of mice with Friend murine leukemia helper virus (F-MuLV). This disease has two separate pathogenic phases both resulting in anemia and splenomegaly. In the first phase virus infection of erythroid precursors causes premature destruction of erythrocytes, giving a hemolytic anemia; splenomegaly results from compensatory erythropoiesis. The second phase consists of erythroleukemia with splenomegaly and anemia due to lack of production and differentiation of erythrocytes. Using two virus variants differing in virulence it was shown that the viral envelope gene was primarily responsible for the induction of early severe hemolytic anemia, whereas the viral LTR region had the main influence on latency of infection of erythroleukemia. Current efforts are aimed at determining the precise gene sequences responsible for each of these effects.