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pubmed:abstractText |
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.
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