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Experimental parainfluenza type 1 virus-induced encephalopathy in adult mice. Pathogenesis of chronic degenerative
Abstract:
The pathogenicity of the 6/94 strain of parainfluenza type 1 virus, originally isolated from multiple sclerosis brain, was studied in adult mouse brains. Intracerebral inoculation of the virus caused mononuclear cell infiltration in the form of perivascular cuffing and a diffuse exudation into the parenchymal tissue, preferentially in cerebral white matter, that resulted in marked degeneration over a 90-day observation period. Immunofluorescent staining revealed viral antigen in the ependymal lining cells only during the first seven days after infection. No correlation was found between the severity of the brain lesions and the level of circulating antiviral antibody, preexisting or newly produced.
Insights
The 6/94 strain of parainfluenza type 1 virus causes brain lesions and degeneration in mice. Viral antigen was detected early, but antibody levels did not correlate with lesion severity.
Area of Science:
- Neurovirology
- Immunology
- Pathology
Background:
- Parainfluenza type 1 virus (PIV-1) has been investigated for potential roles in neurological diseases.
- The 6/94 strain of PIV-1 was originally isolated from a multiple sclerosis (MS) brain, prompting further investigation.
Purpose of the Study:
- To assess the pathogenicity of the PIV-1 6/94 strain in the adult mouse brain.
- To characterize the neuropathological changes induced by PIV-1 infection.
Main Methods:
- Adult mice were intracerebrally inoculated with the PIV-1 6/94 strain.
- Brains were examined over a 90-day period for neuropathological changes.
- Immunofluorescence staining was used to detect viral antigen.
- Circulating antiviral antibody levels were measured.
Main Results:
- Intracerebral inoculation led to mononuclear cell infiltration (perivascular cuffing, diffuse exudation) in the brain, predominantly in white matter.
- Marked brain degeneration was observed within 90 days post-infection.
- Viral antigen was localized to ependymal lining cells during the first week after infection.
- No correlation was found between lesion severity and existing or newly produced antiviral antibodies.
Conclusions:
- The PIV-1 6/94 strain is pathogenic in the adult mouse brain, inducing inflammatory lesions and degeneration.
- Viral antigen presence is transient, and the immune response, as measured by antibody levels, does not appear to correlate with disease severity in this model.