Kinetics of erythroid precursors in mice infected with the anemic or the polycythemic strain of Friend leukemia virus.

Abstract

The kinetics of both erythroid burst-forming and colony-forming units (BFU-E, CFU-E) and myelomonocytic precursors [myelomacrophage colony-forming unit (CFU-C)] have been evaluated in tibial marrow, peripheral blood, and spleen of DBA/2 mice at time intervals after inoculation of either the anemic (FLV-A) or the polycythemic (FLV-P) strain of Friend leukemia virus. Either one of the viruses induced, at 7-10 days after infection, a massive increase in the number of BFU-Es in peripheral blood, in parallel with their depletion in tibial marrow and increase in spleen. A comparable increase in the blood BFU-E number was observed in splenectomized FLV-infected mice. These results indicate a marrow-spleen migration of BFU-Es. In spleen, the increase of the BFU-E number was associated with an increase in the CFU-E pool. In tibial marrow, a sequence of expansion/depletion waves occurred reciprocally at the level of BFU-E and CFU-E. The cycling of BFU-E([(3)H]thymidine in vitro suicide index) in marrow, blood, and spleen was enhanced, whereas that of CFU-E and CFU-C showed little or no modification. These kinetic data suggest that the main target cell of FLV may be the BFU-E or a closely related element. In plates without added erythropoietin (but containing it in fetal calf serum), expression of CFU-E from FLV-P-treated animals was maximal; that of CFU-E from FLV-A-injected mice was either virtually absent or only slight in marrow or spleen, respectively. BFU-E growth always was fully dependent upon erythropoietin addition. Control studies in FLV-infected resistant mice and in susceptible mice given diluted or heat-inactivated virus provide convincing evidence that the phenomena described are induced by FLV.