Peschle C, Migliaccio G, Lettieri F, Migliaccio A R, Ceccarelli R, Barba P, Titti F, Rossi G B
Proc Natl Acad Sci U S A. 1980 Apr;77(4):2054-8. doi: 10.1073/pnas.77.4.2054.
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.
在接种贫血型（FLV-A）或红细胞增多型（FLV-P）Friend白血病病毒后的不同时间间隔，对DBA/2小鼠的胫骨骨髓、外周血和脾脏中的红系爆式集落形成单位和集落形成单位（BFU-E、CFU-E）以及骨髓单核细胞前体[巨噬细胞集落形成单位（CFU-C）]的动力学进行了评估。两种病毒中的任何一种在感染后7-10天，均可诱导外周血中BFU-E数量大幅增加，与此同时，其在胫骨骨髓中的数量减少，在脾脏中的数量增加。在脾切除的FLV感染小鼠中也观察到外周血BFU-E数量有类似增加。这些结果表明BFU-E存在骨髓-脾脏迁移。在脾脏中，BFU-E数量的增加与CFU-E池的增加相关。在胫骨骨髓中，BFU-E和CFU-E水平相互出现一系列扩增/耗竭波。骨髓、血液和脾脏中BFU-E的循环（体外[³H]胸腺嘧啶核苷自杀指数）增强，而CFU-E和CFU-C的循环几乎没有变化或没有变化。这些动力学数据表明，FLV的主要靶细胞可能是BFU-E或与之密切相关的成分。在未添加促红细胞生成素（但胎牛血清中含有促红细胞生成素）的培养皿中，FLV-P处理动物的CFU-E表达最高；FLV-A注射小鼠的CFU-E在骨髓或脾脏中的表达分别几乎不存在或仅轻微表达。BFU-E的生长始终完全依赖于添加促红细胞生成素。对FLV感染的抗性小鼠以及给予稀释或热灭活病毒的易感小鼠进行的对照研究提供了令人信服的证据，表明所描述的现象是由FLV诱导的。
