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Experimental double infection of Japanese encephalitis virus and herpes simplex virus in mouse brain
Abstract:
In our laboratory, 64 autopsy cases of Japanese encephalitis patients were examined by immunofluorescence. Three patients showed some evidences of double infection of Japanese encephalitis virus and herpes simplex virus. Experiments were done to see the mechanisms of double infection. In doubly infected mice, Japanese encephalitis virus antigen was localized in the herpes simplex virus infected areas in the brain. These results suggested that "blood brain barrier" was broken by herpes simplex virus infection and Japanese encephalitis virus gained access to the susceptible cells.
Insights
Herpes simplex virus infection may break the blood-brain barrier, allowing Japanese encephalitis virus to infect brain cells. This study investigated dual infections in autopsy cases and mouse models.
Area of Science:
- Neurovirology
- Infectious Diseases
- Pathology
Background:
- Japanese encephalitis virus (JEV) is a major cause of viral encephalitis globally.
- Herpes simplex virus (HSV) is a common neurotropic virus with known lytic capabilities.
- Co-infections with different viral agents can alter disease pathogenesis.
Purpose of the Study:
- To investigate the potential for dual infection of JEV and HSV in human autopsy cases.
- To elucidate the mechanisms underlying JEV and HSV co-infection in a murine model.
- To determine if HSV infection facilitates JEV entry into the central nervous system.
Main Methods:
- Immunofluorescence staining was used to examine 64 autopsy cases of Japanese encephalitis.
- A murine model was utilized to study the interactions between JEV and HSV.
- Viral antigen localization was assessed in the brains of doubly infected mice.
Main Results:
- Evidence of dual JEV and HSV infection was found in three out of 64 autopsy cases.
- In doubly infected mice, JEV antigens were predominantly found in areas of HSV-induced brain lesions.
- HSV infection appeared to compromise the integrity of the blood-brain barrier.
Conclusions:
- HSV infection may disrupt the blood-brain barrier, creating an entry point for JEV.
- This mechanism could explain the observed dual infections and contribute to severe neurological outcomes.
- Further research is warranted to explore the clinical implications of such viral co-infections.