Murine leukemia virus recombinants that use phosphate transporters for cell entry induce similar spongiform encephalomyelopathies in newborn mice

Virology. 1998 Dec 20;252(2):318-23. doi: 10.1006/viro.1998.9476.

Abstract

Amphotropic Moloney-murine leukemia virus recombinants (Mo-AmphoV) induce a severe spongiform encephalomyelopathy in newborn mice. We show here that a coisogenic recombinant with a 10A1-MuLV host range (Mo-10A1V) also induces a neurodegenerative disease, clinically characterized by mild tremor and ataxia. Spongiform lesions are most severe in the metencephalon and mesencephalon but extend into the prosencephalon and spinal cord. Significantly, the quality of histopathology was indistinguishable between Mo-AmphoV and Mo-10A1V, probably reflecting a final common pathogenic pathway. Common receptor use thus may be an important determinant in the pathogenicity of these viruses. These results have implications for the clinical use of retroviral pseudotypes that use phosphate transporters for cell entry.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Animals
  • Animals, Newborn
  • Brain / pathology
  • Brain / virology
  • Carrier Proteins / physiology*
  • Cell Line
  • Membrane Proteins / physiology*
  • Mice
  • Moloney murine leukemia virus / pathogenicity*
  • Moloney murine leukemia virus / physiology*
  • Phosphate-Binding Proteins
  • Prion Diseases / pathology
  • Prion Diseases / physiopathology
  • Prion Diseases / virology*
  • Receptors, Virus / physiology*
  • Recombination, Genetic
  • Spinal Cord / pathology
  • Spinal Cord / virology
  • Time Factors
  • Transfection
  • Virus Latency

Substances

  • Carrier Proteins
  • Membrane Proteins
  • Phosphate-Binding Proteins
  • Receptors, Virus