Friend murine leukemia virus induces splenic enlargement and an increase in RNA polymerase activity of spleen nuclei. Actinomycin D, administered at 60 µg/kg body weight/day prevents the development of splenomegaly and the elevation of polymerase activity following infection, but it has only a slight effect on the production of virus in spleen tissue. Thus, the alteration of RNA synthesis is not a result of virus proliferation, but instead may be a manifestation of leukemic erythropoiesis. Normal erythropoiesis, stimulated by erythropoietin administration, produces a similar but transient increase in RNA polymerase activity in spleen nuclei. Erythropoietin administered before, but not after, Friend virus infection results in an enhancement of RNA polymerase activity, as measured 9 days after inoculation. This effect is most simply explained by assuming that there is a common target cell pool for both erythropoietin and Friend virus, and that this pool becomes refractory to the influence of the hormone as a result of the leukemic process.


This work was supported by Grant CA 14100 from the National Cancer Institute and by a grant from the United Foundation of Metropolitan Detroit to the Michigan Cancer Foundation.

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