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Sendai virus infection in genetically resistant and susceptible mice
Abstract:
The pathogenesis of Sendai virus infection in genetically resistant (C57Bl/6) and susceptible (DBA/2) nonimmune adult mice was investigated. Rising serum complement-fixation (CF) antibody titers were delayed in DBA/2 mice as compared with C57Bl/6 mice. C57Bl/6 mice developed descending desquamative endobronchiolitis, and DBA/2 mice developed descending proliferative endobronchiolitis and bronchogenic alveolitis. Peribronchiolar lymphoid cuffs that formed in C57Bl/6 mice were thicker and more densely populated than those of DBA/2 mice. Immunofluorescence demonstrated viral antigens confined to the epithelial lining of conducting airways in C57Bl/6 mice but extending to alveolar corner cells in DBA/2 mice. Studies with a transmission electron microscope confirmed that Type II pneumocytes were infected only in DBA/2 mice. IgG-containing cells selectively accumulated along the airways of both strains, but fewer were recruited by DBA/2 mice. These results suggest that genetic resistance to Sendai virus is expressed through the immune system.
Insights
Genetic resistance to Sendai virus in mice involves immune system responses. Resistant mice show faster antibody production and distinct lung inflammation patterns compared to susceptible mice.
Area of Science:
- Virology
- Immunology
- Pathogenesis
Background:
- Sendai virus infection impacts respiratory systems.
- Genetic background influences host response to viral infections.
Purpose of the Study:
- Investigate Sendai virus pathogenesis in genetically resistant (C57Bl/6) and susceptible (DBA/2) mice.
- Determine the role of genetic factors in immune response and lung pathology during infection.
Main Methods:
- Comparative analysis of Sendai virus infection in C57Bl/6 and DBA/2 mice.
- Assessment of serum antibody titers (complement-fixation).
- Histopathological examination of lung tissues (endobronchiolitis, alveolitis, lymphoid cuffs).
- Immunofluorescence and transmission electron microscopy for viral antigen localization and cell tropism.
Main Results:
- DBA/2 mice exhibited delayed complement-fixation antibody titers compared to C57Bl/6 mice.
- Distinct lung pathologies observed: C57Bl/6 mice developed desquamative endobronchiolitis, while DBA/2 mice showed proliferative endobronchiolitis and bronchogenic alveolitis.
- Viral antigens were restricted to airway epithelium in C57Bl/6 mice but extended to alveolar cells (Type II pneumocytes) in DBA/2 mice.
- Peribronchiolar lymphoid cuff formation was more robust in C57Bl/6 mice.
Conclusions:
- Genetic resistance to Sendai virus infection in mice is mediated by the immune system.
- Differences in immune cell recruitment and viral spread correlate with genetic resistance.
- Host genetics significantly dictate the severity and type of lung pathology following Sendai virus infection.