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In vivo selection of two agents differing in hepatoma-inducing activity from strain MC29 avian leukosis virus

Archives of Virology
|January 1, 1981
PubMed

Insights

MC29 virus causes acute leukemia and liver tumors in turkeys. Two variants, "liver" and "bone marrow," show distinct tumor-inducing and leukemogenic activities, suggesting different viral particles may cause leukemia and hepatoma.

Area of Science:

  • Oncology
  • Virology
  • Immunology

Background:

  • MC29 virus is known to induce acute leukemia (myelocytomatosis) and primary liver tumors (hepatomas) in turkey poults.
  • In vivo passages led to the selection of two distinct viral variants: a "liver" variant and a "bone marrow" variant, differing in their ability to induce hepatoma.

Purpose of the Study:

  • To investigate the distinct oncogenic activities of the "liver" and "bone marrow" variants of MC29 virus.
  • To analyze the differences in leukemogenic potential and cellular responses induced by each variant.
  • To examine the kinetics of viral protein (p27) accumulation and the presence of oncogenic viruses in infected turkey organs.

Main Methods:

  • In vivo selection of viral variants through serial passages in turkey poults.
  • Assessment of tumor induction (hepatoma) and leukemogenesis (leukocytosis, lymphocytosis, heteropenia) by each variant.
  • Quantification of viral gs protein (p27) and detection of oncogenic viruses in liver and bone marrow tissues.

Main Results:

  • The "liver" variant induces both hepatoma and acute leukemia, while the "bone marrow" variant induces only acute leukemia.
  • The variants exhibit differential leukemogenic activity, with the "bone marrow" variant causing high-grade leukocytosis and the "liver" variant causing lymphocytosis and heteropenia.
  • Both variants lead to the appearance of primitive myeloid cells in circulation, but differences in oncogenic activity did not correlate with selective viral replication in liver or bone marrow cells.

Conclusions:

  • The distinct oncogenic profiles of the MC29 virus variants suggest that separate viral particles may be responsible for the induction of leukemia and hepatoma.
  • Further research is warranted to elucidate the specific mechanisms by which different viral components contribute to distinct oncogenic outcomes.

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