Spongiform degeneration induced by neuropathogenic murine coronavirus infection

Hiromi Kashiwazaki1, Risa Nomura, Shutoku Matsuyama

  • 1Department of Bioinformatics, Faculty of Engineering, Soka University, Tokyo, Japan.

Insights

A new mouse hepatitis virus (MHV) strain, soluble receptor-resistant mutant 7 (ssr7), causes spongiform encephalopathy in mice. This MHV strain offers a rapid model for studying spongiotic lesion formation in the brain.

Area of Science:

  • Neurovirology
  • Pathology
  • Molecular Biology

Background:

  • Mouse hepatitis virus (MHV) JHMV cl-2 is highly neurovirulent.
  • A novel mutant, soluble receptor-resistant mutant 7 (ssr7), exhibits reduced virulence.
  • ssr7 infection leads to spongiform encephalopathy in mice.

Purpose of the Study:

  • To characterize the neuropathogenesis of the ssr7 MHV strain.
  • To investigate the cellular spread and lesion development in the brain following ssr7 infection.
  • To evaluate ssr7 as a model for infectious spongiform degeneration.

Main Methods:

  • Infection of mice with the ssr7 MHV strain.
  • Histopathological analysis of brain tissue at various time points post-inoculation.
  • Detection of viral antigens and cellular markers (GFAP, nestin).

Main Results:

  • Spongiotic lesions appeared by 2 days post-inoculation and progressed to spongiform encephalopathy by 8-10 days.
  • Initial viral antigen expression was observed in infiltrating monocytes and ependymal cells.
  • Subsequent viral spread occurred in glial fibrillary acidic protein-positive cells and nestin-positive progenitor cells in the subventricular zone (SVZ).
  • Gliosis extended into the brain parenchyma, accompanied by vacuolar degeneration.

Conclusions:

  • The ssr7 strain provides a rapid experimental model for studying spongiotic lesion formation.
  • Viral spread initiates in the SVZ and affects glial progenitor cells.
  • The short incubation period of ssr7-induced encephalopathy is advantageous for mechanistic studies.

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