Role of mink cell focus-inducing virus in leukemias induced by Friend ecotropic virus

Journal of Virology
|June 1, 1984
PubMed

Insights

Friend ecotropic virus (F-Eco) causes leukemia in mice. Mink cell focus-inducing (MCF) viruses are linked to erythroblastosis but not all leukemias, indicating distinct genetic resistance mechanisms in mice.

Area of Science:

  • Virology
  • Immunology
  • Genetics

Background:

  • Recombinant viruses, specifically mink cell focus-inducing (MCF) viruses, are implicated in the pathogenesis of murine leukemias.
  • Friend ecotropic virus (F-Eco) is a long-latency retrovirus known to induce various leukemias in mice.

Purpose of the Study:

  • To investigate the role of MCF viruses in F-Eco-induced leukemias in different mouse strains.
  • To determine the genetic basis for resistance to F-Eco-induced erythroblastosis and its relationship with MCF virus generation.

Main Methods:

  • Neonatal mice of various strains (NFS/N, BALB/c, C57BL) were inoculated with F-Eco.
  • Analysis for the presence of MCF virus and specific DNA restriction enzyme fragments.
  • Experimental inoculation of C57BL mice with F-Eco plus F-MCF mixtures.
  • Genetic crosses between susceptible and resistant mouse strains.

Main Results:

  • MCF virus was detected in NFS/N and BALB/c mice that developed erythroblastosis.
  • MCF virus was not detected in C57BL mice, which were resistant to erythroblastosis but developed other leukemias.
  • C57BL mice inoculated with F-Eco and F-MCF remained resistant to erythroblastosis.
  • Genetic analysis revealed a distinct gene in C57BL mice conferring resistance to erythroblastosis, separate from genes affecting MCF virus generation.

Conclusions:

  • MCF viruses are associated with F-Eco-induced erythroblastosis but are not essential for all F-Eco-induced leukemias.
  • C57BL mice possess a specific gene conferring resistance to F-Eco erythroblastosis, independent of their resistance to MCF virus generation.
  • Murine leukemia pathogenesis involves complex interactions between viral factors and host genetic resistance mechanisms.

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