Transformation of avian lymphoid cells by reticuloendotheliosis virus

Mutat Res. 1988 Jan;195(1):79-90. doi: 10.1016/0165-1110(88)90016-4.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Cell Transformation, Viral*
  • Chickens
  • Defective Viruses / genetics
  • Defective Viruses / physiology
  • Genes, Viral
  • Helper Viruses / genetics
  • Helper Viruses / physiology
  • Leukemia, Experimental / etiology
  • Lymphatic Diseases / etiology
  • Oncogene Proteins v-rel
  • Oncogenes
  • Reticuloendotheliosis virus / genetics
  • Reticuloendotheliosis virus / physiology*
  • Retroviridae / physiology*
  • Retroviridae Proteins / genetics
  • Retroviridae Proteins / physiology*
  • Tumor Virus Infections
  • Turkeys

Substances

  • Oncogene Proteins v-rel
  • Retroviridae Proteins