Lee W H, Bister K, Pawson A, Robins T, Moscovici C, Duesberg P H
Proc Natl Acad Sci U S A. 1980 Apr;77(4):2018-22. doi: 10.1073/pnas.77.4.2018.
The oncogenic properties and RNA of the Fujinami avian sarcoma virus (FSV) and the protein it encodes were investigated and compared to those of other avian tumor viruses with sarcomagenic properties such as Rous sarcoma virus and the acute leukemia viruses MC29 and erythroblastosis virus. Cloned stocks of FSV caused sarcomas in all chickens inoculated and were found to contain a 4.5-kilobase (kb) and an 8.5-kb RNA species. The 4.5-kb RNA was identified as the genome of defective FSV because it was absent from nondefective FSV-associated helper virus and because the titer of focus-forming units increased with the ratio of 4.5-kb to 8.5-kb RNA in virus preparations. This is, then, the smallest known tumor virus RNA with a transforming function. Comparisons with other viral RNAs, based on oligonucleotide mapping and molecular hybridization, indicated that 4.5-kb FSV RNA contains a 5' gag gene-related sequence of 1 kb, an internal specific sequence of about 3 kb that is unrelated to Rous sarcoma virus, MC29, and erythroblastosis virus, and a 3'-terminal sequence of about 0.5 kb related to the conserved C region of avian tumor viruses. The lack of some or all nucleotide sequences of the essential virion genes, gag, pol, and env, and the isolation of FSV-transformed nonproducer cell clones indicated that FSV is replication defective. A 140,000-dalton, gag-related non-structural protein was found in FSV-transformed producer and nonproducer cells and was translated in vitro from full-length FSV RNA. This protein is expected to have a transforming function both because its intracellular concentration showed a positive correlation with the percentage of transformed cells in a culture and because FSV is unlikely to code for major additional proteins since the genetic complexities of FSV RNA and the FSV protein are almost the same. It is concluded that the transforming onc gene of FSV is distinct from that of Rous sarcoma virus and other avian tumor viruses with sarcomagenic properties. Hence, multiple mechanisms exist for sarcomagenic transformation of avian cells.
对藤浪禽肉瘤病毒（FSV）的致癌特性、RNA及其编码的蛋白质进行了研究，并与其他具有肉瘤生成特性的禽肿瘤病毒（如劳氏肉瘤病毒、急性白血病病毒MC29和成红细胞增多症病毒）进行了比较。克隆的FSV毒株在所有接种的鸡中都引发了肉瘤，并且发现其含有4.5千碱基（kb）和8.5 kb的RNA种类。4.5 kb的RNA被鉴定为缺陷型FSV的基因组，因为在无缺陷的FSV相关辅助病毒中不存在该RNA，并且病毒制剂中形成焦点单位的滴度随4.5 kb与8.5 kb RNA的比例增加而升高。因此，这是已知的具有转化功能的最小肿瘤病毒RNA。基于寡核苷酸图谱分析和分子杂交与其他病毒RNA进行比较，结果表明4.5 kb的FSV RNA包含一个1 kb的5' gag基因相关序列、一个约3 kb的与劳氏肉瘤病毒、MC29和成红细胞增多症病毒无关的内部特异性序列以及一个约0.5 kb的与禽肿瘤病毒保守C区域相关的3'末端序列。必需的病毒体基因gag、pol和env的部分或全部核苷酸序列缺失，以及FSV转化的非生产性细胞克隆的分离表明FSV复制存在缺陷。在FSV转化的生产性和非生产性细胞中发现了一种140,000道尔顿的、与gag相关的非结构蛋白，并且该蛋白可在体外从全长FSV RNA翻译获得。预期该蛋白具有转化功能，这是因为其细胞内浓度与培养物中转化细胞的百分比呈正相关，并且由于FSV不太可能编码主要的额外蛋白质，因为FSV RNA和FSV蛋白的遗传复杂性几乎相同。得出的结论是，FSV的转化致癌基因与劳氏肉瘤病毒和其他具有肉瘤生成特性的禽肿瘤病毒的致癌基因不同。因此，禽细胞的肉瘤生成转化存在多种机制。
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