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Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo
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Published on: January 7, 2019

Introduction of a cis-acting mutation in the capsid-coding gene of moloney murine leukemia virus extends its

M Audit1, J Déjardin, B Hohl

  • 1Institut de Génétique Moléculaire de Montpellier (IGMM), IFR24, CNRS-UMR5535, and Université Montpellier II, F-34293 Montpellier Cedex 5, France.

Journal of Virology
|November 13, 1999
PubMed

Insights

A new Moloney murine leukemia virus (MuLV) mutant, MSD1, rapidly induces diverse leukemias in mice, including T-cell lymphomas, erythroid, and myelomonocytic types. This broad oncogenic potential stems from its capsid gene, not the viral enhancer region.

Area of Science:

  • * Retroviral oncogenesis
  • * Murine leukemia virus (MuLV) research
  • * Cancer stem cell biology

Background:

  • * Wild-type Moloney murine leukemia virus (MuLV) exclusively causes T-cell lymphomas.
  • * The T-cell leukemogenic property is linked to the U3 enhancer region of the viral promoter.
  • * A need exists to understand viral mechanisms driving diverse leukemic cell types.

Purpose of the Study:

  • * To investigate a novel Moloney MuLV mutant (MSD1) capable of inducing a broader spectrum of leukemias.
  • * To identify the genetic basis for MSD1's altered leukemogenic potential.
  • * To determine if MSD1's oncogenic activity is linked to the U3 enhancer or capsid gene.

Main Methods:

  • * Inoculation of newborn mice with wild-type (WT) Moloney MuLV and the MSD1 mutant.
  • * Monitoring of leukemic development, latency periods, and phenotypic presentation.
  • * Amplification and sequencing of viral U3 and capsid-coding regions from leukemic spleens.

Main Results:

  • * MSD1 induced leukemias in all inoculated animals with shorter or similar latency compared to WT MuLV.
  • * Only 56% of MSD1-induced leukemias showed the characteristic thymoma phenotype; others were erythroid or myelomonocytic.
  • * The MSD1 mutations in the capsid gene were conserved in leukemic cells, and U3 region changes were not observed.

Conclusions:

  • * MSD1 is the first replication-competent MuLV lacking oncogenes to rapidly cause diverse leukemias.
  • * MSD1's ability to transform erythroid and myelomonocytic lineages is due to a cis-acting effect of the capsid-coding gag sequence.
  • * This finding expands the understanding of retroviral oncogenesis beyond enhancer-driven T-cell transformation.

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