Balduzzi P C, Notter M F, Morgan H R, Shibuya M
J Virol. 1981 Oct;40(1):268-75. doi: 10.1128/JVI.40.1.268-275.1981.
The new avian retroviruses UR1 and UR2 were isolated from spontaneous tumors of chickens by cocultivation of tumor material with susceptible chicken embryo fibroblasts. In vitro, UR1 induced formation of small foci of round and fusiform cells. On the other hand, cells infected by UR2 assumed an extremely elongated morphology. In vivo, both viruses induced fibrosarcomas and myxosarcomas with short latencies. Infectivity assays with and without mitomycin C showed that both viruses were defective for replication, but transformed nonproducing cell clones were obtained only with UR1. UR1-infected transformed nonproducing clones did not release particles detectable by reverse transcriptase assays, and fusion of transformed nonproducing cells with quail cells chronically infected with Rous sarcoma virus (a Bryan strain) failed to rescue infectious virus. This suggested that UR1 does not code for functional envelope glycoproteins. In this regard, UR1 appeared to be similar to Fujinami, PRCII, and Y73 viruses. The helper viruses of partially purified stocks of UR1 and UR2 appeared to belong to subgroup A, but these helper viruses were distinguishable from each other, as shown by host range experiments and neutralization tests. Hybridization studies with DNA complementary to the src gene of Rous sarcoma virus and RNAs extracted from both UR1 and UR2 showed no homology between the genomes of the new isolates and the transforming gene of Rous sarcoma virus.
新型禽逆转录病毒UR1和UR2是通过将肿瘤材料与易感鸡胚成纤维细胞共培养,从鸡的自发肿瘤中分离出来的。在体外,UR1诱导形成圆形和梭形细胞的小病灶。另一方面,受UR2感染的细胞呈现出极其细长的形态。在体内,两种病毒均能在短潜伏期内诱发纤维肉瘤和黏液肉瘤。有无丝裂霉素C的感染性试验表明,两种病毒的复制均存在缺陷,但仅用UR1获得了转化的非生产性细胞克隆。受UR1感染的转化非生产性克隆未释放出可通过逆转录酶检测法检测到的颗粒,并且将转化的非生产性细胞与长期感染劳氏肉瘤病毒(Bryan株)的鹌鹑细胞融合也未能拯救出感染性病毒。这表明UR1不编码功能性包膜糖蛋白。在这方面,UR1似乎与藤浪、PRCII和Y73病毒相似。UR1和UR2部分纯化毒株的辅助病毒似乎属于A亚组,但如宿主范围实验和中和试验所示,这些辅助病毒彼此可区分。用与劳氏肉瘤病毒src基因互补的DNA以及从UR1和UR2中提取的RNA进行杂交研究表明,新分离株的基因组与劳氏肉瘤病毒的转化基因之间没有同源性。