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Genetic resistance to lethal Sendai virus pneumonia: virus replication and interferon production in C57BL/6J and
Abstract:
Resistant C57BL/6J and susceptible DBA/2J mice were exposed to aerosols of Sendai virus and killed at intervals to 12 days. Lungs were removed and assayed for infectious virus and interferon. Mean virus titers were 6 to 400 times higher in DBA/2J mice than in C57BL/6J mice 3 to 10 days after exposure. Mean interferon titers were 10 to 140 times higher in DBA/2J mice than in C57BL/6J mice 4 to 7 days after exposure. These results suggest that genetic resistance to the lethal effects of Sendai virus is expressed through control of viral replication within the first 72 hours of infection and that early expression of inherited resistance is not regulated by interferon.
Insights
Genetic resistance to Sendai virus in C57BL/6J mice involves early control of viral replication, not interferon regulation. Susceptible DBA/2J mice show higher virus and interferon levels, indicating genetic factors influence early infection outcomes.
Area of Science:
- Immunology
- Virology
- Genetics
Background:
- Sendai virus infection causes varying disease severity in different mouse strains.
- Understanding genetic resistance mechanisms is crucial for controlling viral infections.
Purpose of the Study:
- To investigate the genetic basis of resistance to Sendai virus in mice.
- To determine the role of viral replication and interferon in early stages of infection.
Main Methods:
- Exposure of resistant (C57BL/6J) and susceptible (DBA/2J) mice to Sendai virus aerosols.
- Assay of lung tissues for infectious virus and interferon levels at various time points post-exposure.
Main Results:
- DBA/2J mice exhibited significantly higher mean virus titers (6-400 times) compared to C57BL/6J mice from 3 to 10 days post-exposure.
- DBA/2J mice also showed higher mean interferon titers (10-140 times) than C57BL/6J mice between 4 and 7 days post-exposure.
Conclusions:
- Genetic resistance to Sendai virus is primarily mediated by the control of viral replication within the initial 72 hours of infection.
- Early expression of inherited resistance to Sendai virus is independent of interferon regulation.