MacDonald M E, Reynolds F H, Van de Ven W J, Stephenson J R, Mak T W, Bernstein A
J Exp Med. 1980 Jun 1;151(6):1477-92. doi: 10.1084/jem.151.6.1477.
Two distinct clones of Friend spleen focus-forming virus (SFFV), differing in their erythroleukemic potential, are described. These isolates have been cloned free of their associated helper viruses and shown to be replication-defective. Both SFFV isolates have been rescued from rat fibroblast nonproducer cell clones with cloned replication-competent viruses, F-MuLVA and F-MuLVP, obtained from the anemia- or polycythemia-inducing isolates of Friend virus complex, respectively. These rescued viruses induce a rapid proliferative disease associated with the appearance of macroscopic spleen foci and splenomegaly. In addition, each is subject to regulation by the W, Steel (Sl), and Fv-2 host gene loci. These two isolates of SFFV can, however, be distinguished by both biological and molecular criteria. Friend SFFVP induces a rapid polycythemia associated with the appearance of large numbers of erythropoietin (EPO)-independent erythroid colony-forming cells in the marrow and spleen. In contrast, SFFVA induces a rapid anemia associated with a progressive decrease in the number of EPO-dependent erythroid colony-forming cells in marrow, and a rapid increase in the number of EPO-dependent erythroid colony-forming cells in spleen. Furthermore, the nature of the disease induced by the two isolates of SFFV is independent of the Friend helper virus: SFFVP, rescued from a nonproducer cell clone with either F-MuLVA or F0MuLVP, induced a polycythemic transformation, whereas SFFVA, rescued with either F-MuLVA or F-MuLVP, induced an anemic transformation. The two Friend SFFV isolates can also be discriminated on the basis of translational products encoded by their gag and env genes: SFFVP encodes the amino-terminal gag-gene protein p15, whereas SFFVA encodes the gag-gene proteins p15, p12, and p30. In addition, the SFFV isolates encode nonidentical 55,000-mol wt env gene-related proteins that can be distinguished by analysis of their methionine-containing tryptic peptides.
本文描述了两种不同的弗瑞德脾集落形成病毒（SFFV）克隆，它们在致红白血病潜力方面存在差异。这些分离株已克隆去除其相关辅助病毒，并显示为复制缺陷型。两种SFFV分离株均从大鼠成纤维细胞非生产性细胞克隆中拯救出来，所用的具有复制能力的克隆病毒分别是F-MuLVA和F-MuLVP，它们分别来源于弗瑞德病毒复合体的贫血诱导株或红细胞增多症诱导株。这些拯救出的病毒会引发一种快速增殖性疾病，伴有肉眼可见的脾集落出现和脾肿大。此外，每种病毒都受W、Steel（Sl）和Fv-2宿主基因位点的调控。然而，这两种SFFV分离株可通过生物学和分子标准加以区分。弗瑞德SFFVP会引发快速红细胞增多症，伴有骨髓和脾脏中大量不依赖促红细胞生成素（EPO）的红系集落形成细胞出现。相比之下，SFFVA会引发快速贫血，伴有骨髓中依赖EPO的红系集落形成细胞数量逐渐减少，以及脾脏中依赖EPO的红系集落形成细胞数量快速增加。此外，两种SFFV分离株所引发疾病的性质与弗瑞德辅助病毒无关：用F-MuLVA或F0MuLVP从非生产性细胞克隆中拯救出的SFFVP会引发红细胞增多症转化，而用F-MuLVA或F-MuLVP拯救出的SFFVA会引发贫血转化。两种弗瑞德SFFV分离株还可根据其gag和env基因编码的翻译产物进行区分：SFFVP编码氨基末端gag基因蛋白p15，而SFFVA编码gag基因蛋白p15、p12和p30。此外，SFFV分离株编码不同的55,000道尔顿分子量的env基因相关蛋白，可通过分析其含甲硫氨酸的胰蛋白酶肽段加以区分。
