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In vivo effect of three transformation-defective mutants of subgroup C avian sarcoma viruses

Folia Biologica
|January 1, 1980
PubMed

Insights

Three avian sarcoma virus mutants caused hematological disorders resembling erythroblastosis in chickens. One mutant, td daPR-RSV-C, also induced sarcomas, indicating retained oncogenic potential.

Area of Science:

  • Virology
  • Oncology
  • Immunology

Background:

  • Avian sarcoma viruses (ASVs) are retroviruses known to cause tumors in chickens.
  • Transformation-defective (td) mutants of ASVs have lost the ability to transform cells in vitro but may retain oncogenic potential in vivo.
  • Understanding the oncogenic capacity of td mutants is crucial for deciphering viral oncogenesis.

Purpose of the Study:

  • To investigate the in vivo oncogenic potential of three transformation-defective avian sarcoma virus mutants (td PR-RSV-C, td B77, and td daPR-RSV-C).
  • To evaluate the hematological changes and tumor formation induced by these td mutants in chicken embryos and newly-hatched chickens.

Main Methods:

  • Intravenous injection of td PR-RSV-C, td B77, and td daPR-RSV-C into 12-day-old chicken embryos.
  • Intraperitoneal injection of the same td mutants into newly-hatched Brown Leghorn and F1 hybrid chickens.
  • Monitoring of hematological parameters and observation for visible tumor formation over an 8-9 month period.

Main Results:

  • All three td mutants induced hematological disorders in a significant proportion of intraembryonally injected animals.
  • These disorders resembled the anemic and proliferative types of erythroblastosis.
  • The td daPR-RSV-C mutant exhibited the most conspicuous erythroblastosis symptoms and also induced two sarcomas containing transforming viruses.

Conclusions:

  • Transformation-defective avian sarcoma virus mutants can retain significant in vivo oncogenic potential, inducing hematological disorders and tumors.
  • The td daPR-RSV-C mutant demonstrated a notable capacity for inducing both erythroblastosis and sarcomas, suggesting retained or acquired oncogenic information.
  • These findings highlight the complex interplay between viral genetics and host response in avian oncogenesis.

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