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Neuropathological effects of persistent infection of mice by mouse hepatitis virus
Abstract:
Mouse hepatitis virus (MHV3) can persist for months in strains of mice with genetically controlled "semisusceptibility" to this virus. The pathology of the chronic neurological disease induced in these animals has been investigated by conventional histology and immunofluorescence. A2G mice develop a chronic choroidoependymitis and meningitis leading to severe hydrocephalus and hydromyelia. In C3H mice a widespread vasculitis was observed, with both viral antigens and bound immunoglobulins in vessal walls. No significant glomerulonephritis was found. Systemic amyloidosis was present in the spleen, liver, and kidneys. The virus was not detected in neural tissues, but brain and spinal cord lesions were found near inflammatory areas surrounding damaged vessels. It is suggested that viral persistance in ependymal cells is directly responsible for the lesions in A2G mice, whereas an immunopathological lesion of blood vessels of the central nervous system underlines the damage to mice of the C3H strain.
Insights
Mouse hepatitis virus (MHV3) causes chronic neurological disease in susceptible mice. Different mouse strains exhibit distinct pathologies, including inflammation and vasculitis, suggesting varied disease mechanisms.
Area of Science:
- Virology
- Immunology
- Neuropathology
Background:
- Mouse hepatitis virus (MHV3) establishes persistent infections in genetically susceptible mouse strains.
- Chronic neurological disease can develop following MHV3 infection.
Purpose of the Study:
- To investigate the distinct pathological mechanisms of chronic neurological disease induced by MHV3 in different mouse strains.
- To differentiate between direct viral effects and immunopathological responses in MHV3-induced neuropathology.
Main Methods:
- Conventional histology was employed to examine tissue damage.
- Immunofluorescence was used to detect viral antigens and immunoglobulin deposition.
Main Results:
- A2G mice developed chronic choroidoependymitis and meningitis, leading to hydrocephalus and hydromyelia.
- C3H mice exhibited widespread vasculitis with viral antigens and immunoglobulins in vessel walls, alongside systemic amyloidosis.
- No significant glomerulonephritis was observed in C3H mice.
- Neural tissues did not show detectable virus, but lesions were found near inflamed areas surrounding damaged vessels.
Conclusions:
- Viral persistence in ependymal cells is implicated in the A2G mouse neuropathology.
- Immunopathological lesions of central nervous system blood vessels are suggested as the cause of damage in C3H mice.