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Molecular mechanism for retroviral neuropathogenesis: possible involvement of capillary endothelial cells

M Masuda1, M Masuda, S K Ruscetti

  • 1Laboratory of Molecular Oncology, National Cancer Institute, Frederick, Maryland 21702, USA.

Leukemia
|April 1, 1997
PubMed

Insights

A specific strain of Friend Murine Leukemia Virus (MuLV), PVC-211, causes spongiform neurodegeneration by infecting brain capillary endothelial cells (BCEC). Virus targeting of BCEC correlates with disease severity, suggesting BCEC

Area of Science:

  • Virology
  • Neuroscience
  • Immunology

Background:

  • Friend MuLV is a retrovirus known to cause disease in rodents.
  • A specific variant, PVC-211, induces spongiform neurodegeneration.
  • Brain capillary endothelial cells (BCEC) are identified as primary targets of PVC-211 MuLV.

Purpose of the Study:

  • To investigate the role of BCEC tropism in PVC-211 MuLV neuropathogenicity.
  • To explore the mechanisms by which PVC-211 MuLV infection leads to neurodegeneration.

Main Methods:

  • Construction and analysis of chimeric viruses between PVC-211 MuLV and non-neuropathogenic Friend MuLV.
  • Assessment of viral tropism and neuropathological changes in infected rodents.

Main Results:

  • The tropism of PVC-211 MuLV for BCEC was found to correlate directly with its neuropathogenic potential.
  • Infection of BCEC by PVC-211 MuLV is a key factor in inducing spongiform neurodegeneration.

Conclusions:

  • PVC-211 MuLV infects BCEC, which is critical for causing spongiform neurodegeneration.
  • The tropism of the virus for these cells dictates its neuropathogenicity.
  • Cytokine expression by infected BCEC may contribute to neuropathological changes.

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