Tanaka A, Kaji A
J Virol. 1983 Jun;46(3):974-84. doi: 10.1128/JVI.46.3.974-984.1983.
Mutants (PH2010, PH2011, PH2012) of Rous sarcoma virus which have a growth-inhibitory effect on chicken embryo fibroblasts were isolated from a temperature-sensitive mutant of the Schmidt-Ruppin strain of Rous sarcoma virus (tsNY68). The growth rate of fibroblasts infected with these viruses was about 50 to 60% of that of uninfected fibroblasts. A morphological difference between mutant-infected and uninfected fibroblasts was observed at logarithmic phase but not at stationary phase. Neither the protein p60src nor its associated protein kinase activity was significantly detected by an immunoprecipitation assay in the cells infected with these mutants. Analysis of the unintegrated DNA of the mutant PH2010 showed that a sequence of about 1.4 kilobase pairs at the src gene region is deleted. Further examination of the viral structural proteins in infected cells as well as in virions by immunoprecipitation and peptide mapping revealed that the molecular size of the Pr76 gag protein of the mutant RSV is smaller than that of the mutant tsNY68 because of partial deletion at the p19 gag gene. The peptide maps suggest that the deleted region of the altered p19 of the mutant is near the carboxy terminal of p19. The amount of Prgp92env synthesized in the mutant-infected cells was about fivefold more than that in tsNY68-infected cells.
从劳氏肉瘤病毒施密特 - 鲁平株的温度敏感突变体（tsNY68）中分离出了对鸡胚成纤维细胞具有生长抑制作用的劳氏肉瘤病毒突变体（PH2010、PH2011、PH2012）。感染这些病毒的成纤维细胞的生长速率约为未感染成纤维细胞的50%至60%。在对数期观察到突变体感染的和成纤维细胞与未感染的成纤维细胞之间存在形态差异，但在稳定期未观察到。通过免疫沉淀试验，在感染这些突变体的细胞中未显著检测到蛋白p60src及其相关的蛋白激酶活性。对突变体PH2010的未整合DNA分析表明，src基因区域约1.4千碱基对的序列被删除。通过免疫沉淀和肽图谱对感染细胞以及病毒粒子中的病毒结构蛋白进行进一步检查发现，由于p19 gag基因的部分缺失，突变体劳氏肉瘤病毒的Pr76 gag蛋白的分子大小比突变体tsNY68的小。肽图谱表明，突变体改变的p19的缺失区域靠近p19的羧基末端。在突变体感染的细胞中合成的Prgp92env的量比tsNY68感染的细胞中的多约五倍。
