The Fv-2 gene controls induction of erythroid burst formation by Friend virus infection in vitro: studies of growth regulators and viral replication.
The Fv-2 gene controls induction of erythroid burst formation by Friend virus infection in vitro: studies of growth regulators and viral replication.
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Fv-2 基因在体外控制弗兰德病毒感染诱导红系爆发形成：生长调节剂和病毒复制的研究。
DOI：
10.1099/0022-1317-66-1-83
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Krantz,SB
中科院分区：
文献类型：
--
作者：
Bondurant,MC;Koury,MJ;Krantz,SB
当用Friend病毒复合物体外感染时，易感小鼠的骨髓细胞在半固体培养基中培养5天后形成大的成红细胞集落（爆发）。这种病毒诱导的爆发式生长发生在不添加促红细胞生成素（EP）的情况下，而促红细胞生成素通常是体外红系祖细胞生长所需的。来自Friend病毒体外感染的C57 BL/6小鼠的红系祖细胞对病毒诱导的爆发性生长有抵抗力，而来自B6.与C57 BL/6同源但在Fv-2位点上具有Friend病毒敏感性等位基因的S系小鼠是易感的。B6的这种易感性。S细胞表明病毒诱导的爆发生长受Fv-2基因调控。分析了Fv-2位点控制病毒抗性的两种机制。检测了可溶性物质对病毒的红细胞增殖效应的可能调节，所述可溶性物质促进敏感菌株的爆发生长或抑制抗性菌株的生长。此外，可能的限制病毒感染或复制的抗性（Fv-2 rr）造血细胞进行了研究。在各种实验条件下，可溶性生长促进剂对体外感染的骨髓细胞的影响均不能克服C57 BL/6细胞对红系爆发形成的抵抗。C57 BL/6细胞在培养过程中产生的任何可溶性物质也不能将抗性转移到共培养的敏感细胞。在造血的各种生理状态下使用来自C57 BL/6动物的造血细胞也没有克服对病毒诱导的爆发性生长的抗性。对全骨髓培养物或Fv-2敏感和Fv-2抗性同源小鼠品系爆发的成红细胞中病毒复制的几个参数进行定量分析表明，两种品系的造血细胞同样支持病毒生长。这些数据表明，Fv-2 rr介导的对Friend病毒感染的红细胞增殖效应的抵抗是红系祖细胞靶细胞的固有特性，而不是由外部因素决定的。抗性也不是由于病毒复制的限制。
When infectedin vitrowith Friend virus complex, the bone marrow cells of susceptible mice form large colonies (bursts) of erythroblasts after 5 days of culture in semi-solid medium. This virus-induced burst growth occurs without the addition of erythropoietin (EP) which is normally required for erythroid progenitor growthin vitro. Erythroid progenitor cells from C57BL/6 mice infectedin vitrowith Friend virus are resistant to virus-induced burst growth, while cells from the B6. S mouse strain, which is congenic with C57BL/6 but possesses the ‘Friend virus sensitivity’ alleles at theFv-2locus, are susceptible. This susceptibility of the B6. S cells demonstrates that virus-induced burst growth is regulated by theFv-2gene. Two mechanisms by which theFv-2locus could control virus resistance were analysed. The possible modulation of the erythroproliferative effect of the virus by soluble substances which either promote burst growth in the sensitive strains or inhibit growth in the resistant strain was examined. Also, the possible restriction of virus infection or replication in resistant (Fv-2rr) haemopoietic cells was investigated. In a variety of experimental conditions designed to test the effects of soluble growth promoters on bone marrow cells infectedin vitro, the resistance of C57BL/6 cells to erythroid burst formation could not be overcome. Neither could resistance be transferred to co-cultured sensitive cells by any soluble substances produced in culture by C57BL/6 cells. Use of haemopoietic cells from C57BL/6 animals in various physiological states of haemopoiesis also did not overcome the resistance to virus-induced burst growth. Quantification of several parameters of viral replication in whole marrow cultures or in erythroblasts from bursts of theFv-2sensitive andFv-2resistant congenic mouse strains showed that haemopoietic cells of both strains support virus growth equally well. These data suggest thatFv-2rr-mediated resistance to the erythroproliferative effect of Friend virus infectionin vitrois an inherent property of an erythroid progenitor target cell and is not determined by external factors. The resistance is also not due to restriction of virus replication.