Kaminchik J, Hankins W D, Ruscetti S K, Linemeyer D L, Scolnick E M
J Virol. 1982 Dec;44(3):922-31. doi: 10.1128/JVI.44.3.922-931.1982.
Previously, we have molecularly cloned proviral DNA of a polycythemia-inducing strain of the spleen focus-forming virus (SFFVp). In this paper, we report that unintegrated proviral DNA of the anemia-inducing strain of SFFV (SFFVA) has been molecularly cloned into pBR322. This molecularly cloned DNA retains the biological activity of SFFVA, as infectious SFFV can be recovered from the DNA clone by marker rescue using a previously described two-stage cotransfection assay (Linemeyer et al., J. Virol. 35:710-721, 1980). The recovered SFFV retains an important property of the initial SFFVA which distinguishes SFFVA from SFFVP, namely, the ability of SFFVA to cause proliferation of erythroid cells in which hemoglobin synthesis is erythropoietin dependent. By utilizing a marker rescue technique, the splenomegaly and anemia characteristic of SFFVA-induced disease have been traced to a DNA fragment of SFFVA containing sequences coding for the env gene product. gp52. The results suggest that the differences in pathogenicity between SFFVP disease and SFFVA disease are an intrinsic property of the env gene products of these two variants of Friend virus, and future studies with the molecular clones of each strain should allow us to map regions of each env gene responsible for common and distinctive features of the erythroproliferative diseases induced by each virus.
此前，我们已对脾灶形成病毒（SFFVp）的一种诱导红细胞增多症毒株的前病毒DNA进行了分子克隆。在本文中，我们报告了SFFV的贫血诱导毒株（SFFVA）的未整合前病毒DNA已被分子克隆到pBR322中。这种分子克隆的DNA保留了SFFVA的生物学活性，因为通过使用先前描述的两阶段共转染试验（Linemeyer等人，《病毒学杂志》35:710 - 721，1980）进行标记拯救，可以从DNA克隆中回收有感染性的SFFV。回收的SFFV保留了初始SFFVA的一个重要特性，该特性将SFFVA与SFFVP区分开来，即SFFVA能够使血红蛋白合成依赖于促红细胞生成素的红系细胞增殖。通过利用标记拯救技术，已将SFFVA诱导疾病的脾肿大和贫血特征追溯到SFFVA的一个包含编码env基因产物gp52序列的DNA片段。结果表明，SFFVP疾病和SFFVA疾病之间致病性的差异是Friend病毒这两种变体的env基因产物的内在特性，并且对每种毒株分子克隆的进一步研究应能使我们绘制出每个env基因中负责每种病毒诱导的红系增殖性疾病的共同和独特特征的区域。
