Characterization of some isolates of newly recovered avian sarcoma virus

Journal of Virology
|January 1, 1979
PubMed

Insights

Newly recovered avian sarcoma virus (rASV) was generated from transformation-defective (td) Rous sarcoma virus mutants in chickens. These rASV isolates regained src gene information, suggesting a genetic interaction with host cells.

Area of Science:

  • Virology
  • Molecular Biology
  • Oncology

Background:

  • Avian sarcoma viruses (ASVs) are retroviruses known to cause tumors in chickens.
  • Transformation-defective (td) mutants of Rous sarcoma virus (RSV) have deletions in the viral oncogene, src.
  • Previously, a recovered ASV (rASV) was isolated from tumors induced by td mutants.

Purpose of the Study:

  • To further characterize the biological and biochemical properties of newly recovered avian sarcoma viruses (rASV).
  • To investigate the genetic basis for the recovery of sarcoma virus activity from transformation-defective mutants.

Main Methods:

  • Cocultivation of tumor cells with chicken embryo fibroblasts and tissue homogenization to obtain high titers of rASV.
  • Analysis of viral growth characteristics, subgroup specificity, and structural protein electrophoresis.
  • Molecular hybridization using src-specific complementary DNA (cDNAsrc) to assess genetic information in viral RNA.

Main Results:

  • Most rASV isolates exhibited non-defective replication and characteristics similar to the parental Schmidt-Ruppin strain of RSV, subgroup A (SR-RSV-A).
  • rASV genomic RNA was larger than parental td RNA and indistinguishable in size from SR-RSV-A.
  • Molecular hybridization revealed that rASV had regained significant portions of the src gene absent in the td mutants.

Conclusions:

  • The recovered avian sarcoma viruses (rASV) have reacquired genetic information, specifically within the src gene, that was deleted in the transformation-defective mutants.
  • The generation of rASV likely involves a genetic recombination or interaction between the transformation-defective virus and host cell genetic material.
  • These findings provide insights into viral evolution and oncogene restoration mechanisms.