Wang L H, Moscovici C, Karess R E, Hanafusa H
J Virol. 1979 Nov;32(2):546-56. doi: 10.1128/JVI.32.2.546-556.1979.
Tumors were produced in quails about 2 months after injection with a transformation-defective mutant of the Schmidt-Ruppin strain of Rous sarcoma virus, subgroup A (SR-A), that retains a small portion of the src gene. Sarcoma viruses were isolated from each of five such tumors. A transformation-defective mutant which has a nearly complete deletion of the src gene was unable to induce tumors. The avian sarcoma viruses recovered from quail tumors (rASV-Q) had biological properties similar to those of the avian sarcoma viruses previously acquired from chicken tumors (rASV-C); these chicken tumors had been induced by the same transformation-defective mutants. Both rASV-Q and rASV-C transformed cells in culture with similar focus morphology and produced tumors within 7 to 14 days after injection into chickens or quails. The size of rASV-Q genomic RNA was indistinguishable from that of SR-A by polyacrylamide gel electrophoresis. The sequences of rASV-Q RNA genomes were analyzed and compared with those of the parental transformation-defective virus, SR-A and of rASV-C by RNase T1 fingerprinting and oligonucleotide mapping. We found that the src sequences of all five isolates of rASV-Q were identical to each other but different from those of SR-A and rASV-C. Of 13 oligonucleotides of rASV-Q identified as src specific, two were not found in either SR-A or rASV-C RNA. Furthermore, some oligonucleotides present in SR-A or rASV-C or both were absent in rASV-Q. No differences were found for the sequences outside the src region in any of the viruses examined. In addition, rASV-Q-infected cells possessed a 60,000-dalton protein specifically precipitable by rabbit serum raised against SR-D-induced tumors. The facts that the src sequences are essentially the same for rASV's recovered from one animal species and different for rASV's obtained from different species provide conclusive evidence that cellular sequences of normal birds were inserted into the viral genome and supplied to the resulting recombinant viruses genetic information for cell transformation.
在用罗氏肉瘤病毒A亚组（SR - A）的施密特 - 鲁平株的转化缺陷型突变体注射鹌鹑约2个月后产生了肿瘤，该突变体保留了src基因的一小部分。从五个这样的肿瘤中分别分离出肉瘤病毒。一个src基因几乎完全缺失的转化缺陷型突变体无法诱导肿瘤。从鹌鹑肿瘤中回收的禽肉瘤病毒（rASV - Q）具有与先前从鸡肿瘤中获得的禽肉瘤病毒（rASV - C）相似的生物学特性；这些鸡肿瘤是由相同的转化缺陷型突变体诱导产生的。rASV - Q和rASV - C在培养物中转化细胞时具有相似的集落形态，并且在注射到鸡或鹌鹑体内7至14天后产生肿瘤。通过聚丙烯酰胺凝胶电泳，rASV - Q基因组RNA的大小与SR - A的无法区分。通过核糖核酸酶T1指纹图谱和寡核苷酸图谱分析了rASV - Q RNA基因组的序列，并将其与亲本转化缺陷型病毒SR - A和rASV - C的序列进行了比较。我们发现rASV - Q的所有五个分离株的src序列彼此相同，但与SR - A和rASV - C的不同。在被鉴定为src特异性的rASV - Q的13个寡核苷酸中，有两个在SR - A或rASV - C RNA中均未发现。此外，SR - A或rASV - C或两者中存在的一些寡核苷酸在rASV - Q中不存在。在所检查的任何病毒中，src区域外的序列均未发现差异。此外，rASV - Q感染的细胞具有一种60,000道尔顿的蛋白质，该蛋白质可被针对SR - D诱导的肿瘤产生的兔血清特异性沉淀。从一种动物物种回收的rASV的src序列基本相同，而从不同物种获得的rASV的src序列不同，这些事实提供了确凿的证据，表明正常鸟类的细胞序列被插入到病毒基因组中，并为产生的重组病毒提供了细胞转化的遗传信息。
