title: Transformation of avian lymphoid cells by reticuloendotheliosis virus.
abstract: Avian reticuloendotheliosis virus (REV-T) is the most virulent of all retroviruses, inducing an invariably fatal leukemia in chickens with a latent period of 7-10 days. Unlike avian cells transformed by other acutely transforming viruses, lymphoid cells transformed by REV-T are immortalized. Furthermore, in vitro derived, REV-T transformed cells which do not produce virus are tumorigenic and induce lethal reticuloendotheliosis when injected into histocompatible birds. Thus REV-T transforms its target cell both in vitro and in vivo. In addition this transformation is independent of any helper virus functions. Like other acute leukemia viruses, REV-T is replication-defective and must co-replicate with a reticuloendotheliosis associated virus (REV-A). During evolution, a substantial portion of its genome has been deleted and replaced with a host-derived genetic sequence, designated v-rel. Presumably, the v-rel oncogene was transduced from a normal turkey DNA locus, c-rel. There are 9 regions of homology between c-rel and v-rel, however, several differences exist between these genes, suggesting that transformation by REV-T results from the production of an altered v-rel protein. The v-rel sequence is distinct from other known oncogenes and encodes a 57-kDa phosphoprotein. In REV-T transformed cells, this pp57v-rel protein is localized in the cytoplasm. The product of the v-rel oncogene is present at a low level, representing only about 0.003% of total methionine-labelled protein. In addition, pp57v-rel is relatively stable, having an estimated half-life of 4-10 h. The v-rel protein when purified close to homogeneity is complexed with a 40-kDa cellular phosphoprotein in transformed lymphoid cells and possesses serine kinase activity. This review discusses the molecular aspects of transformation by REV-T in the context of other oncogene-encoded proteins.
authors.affiliation: Department of Microbiology, University of Texas at Austin 78712-1095.
authors.forename: B E
authors.initials: BE
authors.lastname: Moore
authors.forename: H R
authors.initials: HR
authors.lastname: Bose
mesh_terms: D000818:Animals; D002472:Cell Transformation, Viral; D002645:Chickens; D003673:Defective Viruses / Q000235:genetics / Q000502:physiology; D005814:Genes, Viral; D006378:Helper Viruses / Q000235:genetics / Q000502:physiology; D007942:Leukemia, Experimental / Q000209:etiology; D008206:Lymphatic Diseases / Q000209:etiology; D020572:Oncogene Proteins v-rel; D009857:Oncogenes; D001356:Reticuloendotheliosis virus / Q000235:genetics / Q000502:physiology*; D012190:Retroviridae / Q000502:physiology*; D012191:Retroviridae Proteins / Q000235:genetics / Q000502:physiology*; D014412:Tumor Virus Infections; D014422:Turkeys
chemical_list: D020572:Oncogene Proteins v-rel; D012191:Retroviridae Proteins