ROLE OF ENDOGENOUS AND RECOMBINANT RETROVIRUSES IN LEUKEMIA AND DIFFERENTIATION

本课题旨在探讨骨质疏松症的发病机制。 小鼠白血病病毒。Friend小鼠白血病辅助病毒(F-MuLV) 诱导早期溶血性贫血(EHA)，接种后三周 新生的小鼠。相比之下，Moloney鼠白血病病毒(M-MuLV)则不 诱发严重的EHA。为了定义F-MuLV的哪些部分和 M-MuLV基因组是导致EHA诱导差异的原因。 重组逆转录病毒被构建为交换不同部分的 F-MuLV和M-MuLV的基因组。结果表明，只有 含有F-MuLV U5-Gag-Pol区的逆转录病毒可诱导EHA。 该区域与EHA发病相关的精确序列 现在被定义为构建更多的重组逆转录病毒 和定点突变。

This project is aimed at investigation of mechanisms of pathogenesis of murine leukemia viruses. The Friend murine leukemia helper virus (F-MuLV) induces early hemolytic anemia (EHA) three weeks post inoculation of newborn mice. In contrast, Moloney murine leukemia virus (M-MuLV) does not induce severe EHA. In order to define which portions of the F-MuLV and M-MuLV genomes were responsible for the differences in induction of EHA, recombinant retroviruses were constructed exchanging different portions of the genomes of F-MuLV and M-MuLV. The results indicated that only retroviruses containing the U5-gag-pol region of F-MuLV could induce EHA. The precise sequence in this region responsible for the pathogenesis of EHA is now being defined by construction of additional recombinant retroviruses and sitespecific mutagenesis.