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  • Title: Host control of endogenous murine leukemia virus gene expression: concentrations of viral proteins in high and low leukemia mouse strains.
    Author: Strand M, Lilly F, August JT.
    Journal: Proc Natl Acad Sci U S A; 1974 Sep; 71(9):3682-6. PubMed ID: 4372631.
    Abstract:
    Two of the major molecular components of murine leukemia virus particles, the internal protein (p30) and the envelope glycoprotein (gp69/71) have been measured in the spleens of normal, 6- to 10-week-old mice of various inbred strains and crosses. Both proteins were detected in virtually all mice. Extracts of high leukemia, high murine leukemia virus strains (AKR, C58, PL) showed high levels of both proteins; extracts of other strains usually showed lower levels. Of particular interest, however, were the exceptions to these general observations: (1) Very little gp69/71 could be detected in spleens of BALB mice, and this trait was dominant in crosses with AKR and DBA/2, both of which express a high level of gp69/71. Thymus-deficient BALB/c-nu/nu (nude) mice, in contrast, showed a higher concentration of gp69/71 typical of other low leukemia strains, suggesting that the virtual absence of the protein in normal BALB/c mice may result from immunologic suppression. (2) With C57L, C57BL/10Sn, and C57BL/6 strains the concentration of p30 was lower, in some cases much lower, than would be expected from the concentration of gp69/71. (3) DBA/2 mice showed high levels of gp69/71, 10-fold greater than that of p30, whereas congenic DBA/2-Fv-1(b) mice showed the opposite pattern. (4) Mice of 129-G(IX) (-) strain showed no detectable levels of either p30 or gp69/71 proteins, although the congenic 129 (G(IX) (+)) showed appreciable levels of both. The absence of these proteins in 129-G(IX) (-) mice is a recessive trait, as F(1) hybrids with AKR and DBA/2 showed appropriate levels of both proteins. It is concluded that expression of viral p30 and gp69/71 proteins in mice is not coordinately linked and that expression is complex, being influenced by several genes, including Gv-1, H-2, Fv-1, and probably still others.
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