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Enhanced resistance against Junin virus infection induced by Corynebacterium parvum
Abstract:
The effects of intraperitoneal administration of Corynebacterium parvum on the course of Junin virus infection in mice were investigated. This treatment produced enhanced resistance to the virus infection, evidenced by an increase in both survival times and the proportion of survivors. The protective effect was dependent upon the dose of C. parvum, and 280 mug/g of body weight was found to be the optimal dose. In various experiments, about 80% of the infected animals receiving this dose survived, whereas survival ranged between 0 and 20% among untreated infected mice. Maximal protection was afforded by C. parvum when administered simultaneously with the virus. A smaller but significant degree of resistance was induced by C. parvum given 3 or 6 days after infection. C. parvum injected before infection was ineffective. Viral titers measured in the brains of C. parvum-treated and untreated mice at various times after infection were found to be comparable. In addition, there were no significant differences between circulating-antibody titers measured either by neutralization tests or by complement fixation. Depression of the reticuloendothelial system by treatment with silica particles also resulted in enhanced resistance to Junin virus infection, suggesting that the protective effect of C. parvum is not likely to be due merely to its capacity to stimulate macrophages. The present data, highlighting that the presence of high titers of Junin virus and disease do not necessarily correlated, suggest that in mice this disease is not the consequence of cell damage caused directly by the virus but of a still undefined indirect mechanism induced by the virus, not necessarily mediated by macrophages.
Insights
Corynebacterium parvum treatment enhances resistance to Junin virus infection in mice. Optimal protection occurred when administered with the virus, suggesting indirect mechanisms, not macrophage stimulation, are involved.
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- Junin virus causes severe disease in mice.
- The role of immune stimulation in Junin virus infection is not fully understood.
Purpose of the Study:
- To investigate the effects of Corynebacterium parvum (C. parvum) on Junin virus infection in mice.
- To determine the optimal dose and timing of C. parvum administration for protective effects.
- To elucidate the mechanism underlying C. parvum-mediated protection.
Main Methods:
- Intraperitoneal administration of varying doses of C. parvum to mice infected with Junin virus.
- Assessment of survival rates, survival times, viral titers in brain tissue, and antibody responses.
- Comparison with C. parvum treatment timing and effects of reticuloendothelial system blockade with silica particles.
Main Results:
- C. parvum administration significantly increased survival rates and prolonged survival times in a dose-dependent manner, with 280 mug/g being optimal.
- Maximal protection was achieved when C. parvum was given simultaneously with the virus; delayed administration showed partial protection, while pre-infection treatment was ineffective.
- Viral and antibody titers in the brain were comparable between treated and untreated groups, and C. parvum's protective effect was not solely due to macrophage stimulation, as silica treatment also enhanced resistance.
Conclusions:
- C. parvum confers significant protection against Junin virus infection in mice, primarily when administered concurrently with the virus.
- The protective mechanism appears to be indirect and not solely mediated by macrophage activation.
- Junin virus disease in mice may result from an undefined indirect mechanism rather than direct viral-induced cell damage.