Prenatal transmission and pathogenicity of endogenous ecotropic murine leukemia virus Akv

I Hesse1, A Luz, B Kohleisen

  • 1Institute of Molecular Virology, GSF-National Research Center for Environment and Health, Neuherberg, Germany.

Laboratory Animal Science
|November 7, 1999
PubMed
Abstract

Insights

Prenatal exposure to murine leukemia viruses (MuLV) in dams readily infects embryos, leading to increased embryo lethality. Inappropriate expression of these endogenous retroviruses during gestation is linked to embryo death and reduced breeding success in mice.

Area of Science:

  • Virology
  • Immunology
  • Developmental Biology

Background:

  • Endogenous ecotropic murine leukemia viruses (MuLV) can be expressed throughout life in mice.
  • Transplacental transmission of MuLV poses risks of embryo infection and pathogenic effects.
  • Postnatal MuLV infection is associated with tumorigenesis.

Purpose of the Study:

  • To investigate the impact of maternal MuLV viremia on embryonic development and survival.
  • To determine the role of prenatal MuLV infection and expression in embryo lethality.
  • To assess the long-term effects of MuLV infection on tumor development in mice.

Main Methods:

  • Implantation of MuLV-negative embryos into MuLV-infected or control dams.
  • Analysis of virus integration and expression in embryos at 14 days' gestation.
  • Monitoring of tumor development over 18 months post-birth.

Main Results:

  • Embryos from MuLV-viremic dams showed higher infection rates and increased lethality, significantly associated with prenatal provirus expression.
  • Prenatal MuLV infection and expression were linked to embryo death.
  • Postnatal MuLV infection significantly increased the incidence of lymphoblastic lymphomas compared to controls.

Conclusions:

  • Embryos gestated in MuLV-viremic dams are susceptible to infection.
  • Inappropriate prenatal expression of endogenous retroviruses contributes to embryo lethality and impaired reproductive performance.
  • MuLV infection is a significant risk factor for tumorigenesis in mice.