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Two separate envelope regions influence induction of brain disease by a polytropic murine retrovirus (FMCF98)

K J Hasenkrug1, S J Robertson, J Porti

  • 1Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840, USA. Kim Hasenkrug@rml.niaid.pc.niaid.nih.gov

Journal of Virology
|July 1, 1996
PubMed

Insights

Researchers identified key viral envelope gene regions responsible for causing neurological disease in mice. These findings advance understanding of polytropic murine leukemia virus (MLV) pathogenesis and neurovirulence.

Area of Science:

  • Virology
  • Neuroscience
  • Molecular Biology

Background:

  • Polytropic murine leukemia virus (MLV) can cause neurological diseases.
  • The envelope gene of MLV is crucial for its neurovirulence.

Purpose of the Study:

  • To further map the specific determinants within the MLV envelope gene responsible for inducing neurological disease.
  • To investigate the roles of different envelope gene regions in MLV neurovirulence.

Main Methods:

  • Construction and analysis of four chimeric polytropic MLV viruses.
  • Combining envelope gene sequences from neurovirulent (FMCF98) and non-neurovirulent (FMCF54) strains.
  • Clinical observation of induced neurological signs in mice.
  • Western blot and immunohistochemical analyses of viral expression in brain tissues.

Main Results:

  • Two chimeric viruses, each containing distinct FMCF98 envelope regions, induced neurological disease.
  • Clinical signs were similar to the parent FMCF98 strain, but with longer incubation periods.
  • One neurovirulence determinant was located in the N-terminal gp70, including VRA and VRB regions.
  • A second determinant was mapped downstream of these variable regions.
  • Viral expression levels and localization in the brain did not explain the observed neurovirulence variations.

Conclusions:

  • The MLV envelope gene contains multiple, distinct determinants that contribute to neurovirulence.
  • These determinants can function independently to induce neurological disease.
  • Neurovirulence is not solely dependent on the quantitative or spatial expression of the virus in the brain.

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