The prelymphoid leukemic phase of Rauscher leukemia virus (RLV) infection is characterized by erythroblastosis, reticulocytosis, splenomegaly, and anemia. Reticulocyte counts increased, and RBC, hematocrit, and hemoglobin levels decreased progressively until the 29th day after RLV inoculation. Splenic and hepatic δ-aminolevulinic acid synthetase activity, on a per g tissue basis, decreased compared with normal activity. However, since the spleen increased to 25 times its normal size, the net δ-aminolevulinic acid synthetase activity increased 1340% compared with normal spleen activity. In contrast, mice treated with phenylhydrazine, a drug which causes hemolytic anemia, showed a threefold normal increase in the specific activity of splenic δ-aminolevulinic acid synthetase but showed only a small increase in spleen size. These findings suggest that the RLV-induced anemia does not trigger the same erythropoietic response as does the drug-induced anemia.

Since erythropoietin (ESF) mediates RBC production, the role of this hormone in RLV infection was examined. Low levels of ESF were found in plasma from mice infected with RLV for 7 to 35 days, but the ESF activity was inappropriate for the extent of the anemia. Bleeding of RLV-infected mice to stimulate ESF production did not elicit any response. The possibility that RLV, like the Friend virus, may stimulate erythropoiesis in the absence of ESF production is discussed.

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Portions of this work have been presented (8).

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