Related Experiment Video
Updated: Jun 3, 2026

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
Published on: April 28, 2019
Spongiform degeneration induced by neuropathogenic murine coronavirus infection
Hiromi Kashiwazaki1, Risa Nomura, Shutoku Matsuyama
1Department of Bioinformatics, Faculty of Engineering, Soka University, Tokyo, Japan.
Abstract:
Soluble receptor-resistant mutant 7 (ssr7) is isolated from a highly neurovirulent mouse hepatitis virus (MHV) JHMV cl-2 strain (cl-2). srr7 exhibits lower virulence than its maternal strain in infected mice, which is typically manifested in a longer lifespan. In this study, during the course of infection with srr7, small spongiotic lesions became apparent at 2 days post-inoculation (pi), they spread out to form spongiform encephalopathy by 8 to 10 days pi. We recently reported that the initial expressions of viral antigens in the brain are detected in the infiltrating monocyte lineage and in ependymal cells. Here, we demonstrate that the next viral spread was observed in glial fibrillary acidic protein-positive cells or nestin-positive progenitor cells which take up positions in the subventricular zone (SVZ). From this restricted site of infection in the SVZ, a large area of gliosis extended deep into the brain parenchyma where no viral antigens were detected but vacuolar degeneration started at 48 h pi of the virus. The extremely short incubation period compared with other experimental models of infectious spongiform degeneration in the brain would provide a superior experimental model to investigate the mechanism of spongiotic lesions formation.
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.
Related Concept Videos
Coronavirus
Viral Meningitis
Encephalitis ll: Pathophysiology
Arboviral Encephalitis
Bacterial Meningitis II: Pathophysiology

