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Age dependent susceptibility to Reovirus type 3 encephalitis: role of viral and host factors
Abstract:
Reovirus type 3 inoculated intracerebrally or subcutaneously into newborn mice induced an acute necrotizing and uniformly fatal encephalitis. Subsequently, between the eighth and tenth day of age, reovirus type 3 infection changed to a nonlethal infection. This pattern of virulence was directly correlated with the ability of the virus to replicate in the brain and histologically was accompanied by a gradual diminution in the intensity and extent of encephalitis such that histological abnormalities were absent in the brains of virus-injected adult animals. Some animals injected at ages 10 to 18 days developed brainstem and diencephalic lesions, indicating a nonuniform resistance of neurons to viral infection with aging. Neither a changing immune response pattern nor a modification or loss of viral receptors appears to explain either the susceptibility of newborn or the resistance of adult animals to reovirus type 3 encephalitis. Splenic mononuclear cells from mice younger (but not older) than 7 days also permitted reovirus type 3 replication in vitro. Thus, the age dependent resistance to reovirus type 3 encephalitis appears related to an intrinsic resistance to viral replication by neuronal cells, a resistance that may occur simultaneously in nonneuronal cell populations.
Insights
Newborn mice infected with reovirus type 3 develop fatal encephalitis, but older mice resist infection. This age-dependent resistance is linked to intrinsic neuronal cell resistance to viral replication, not immune response changes.
Area of Science:
- Virology
- Neuroscience
- Immunology
Background:
- Reovirus type 3 infection in newborn mice causes severe, fatal encephalitis.
- This virulence diminishes significantly in older mice, suggesting age-related resistance mechanisms.
Purpose of the Study:
- To investigate the age-dependent susceptibility and resistance of mice to reovirus type 3 encephalitis.
- To elucidate the underlying mechanisms, including viral replication and cellular responses, contributing to this age-related difference.
Main Methods:
- Intracerebral and subcutaneous inoculation of reovirus type 3 into mice of varying ages.
- Histological examination of brain tissue to assess encephalitis severity and extent.
- In vitro replication assays using splenic mononuclear cells from mice of different ages.
Main Results:
- Newborn mice exhibited acute, fatal encephalitis, while mice infected after 8-10 days showed nonlethal infections.
- Viral replication in the brain correlated with encephalitis severity, decreasing with age.
- Neuronal cells in older mice demonstrated intrinsic resistance to viral replication, a phenomenon also observed in non-neuronal cells.
Conclusions:
- Age-dependent resistance to reovirus type 3 encephalitis is primarily due to intrinsic neuronal cell resistance to viral replication.
- This intrinsic resistance, rather than immune system changes or receptor alterations, dictates the outcome of infection.
- The findings highlight the critical role of cellular intrinsic factors in determining viral pathogenesis and host susceptibility.