ROLE OF ENDOGENOUS AND RECOMBINANT RETROVIRUSES IN LEUKEMIA AND DIFFERENTIATION

本项目旨在探讨其发病机制

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.