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Immunostimulation in mice infected with Sendai virus
1Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06510.
Abstract:
The effect of Sendai virus infection on the splenic primary plaque-forming cell (PFC) response to sheep RBC in 2 strains of mice, with contrasting susceptibility to Sendai viral pneumonia, was examined. Mice were given single inoculations of sheep RBC, which varied relative to time of inoculation with Sendai virus, PFC were counted 6 days later, and were compared with PFC responses from noninfected mice. The IgM- and IgG-PFC responses were augmented in resistant C57BL/6J mice 7 and 9 days after inoculation with Sendai virus (sheep RBC given 1 and 3 days after inoculation with Sendai virus, respectively) and in susceptible DBA/2J mice 7, 9, 10, and 13 days after inoculation with Sendai virus. Augmentation was restricted mainly to IgM-, IgG3-, and IgG2b-PFC. The number of splenic background antitrinitrophenyl sheep RBC PFC in mice of both strains was examined during the course of Sendai virus infection. Only a marginal increase in background PFC was seen in C57BL/6J mice on or after viral inoculation day 11 and no change was seen in DBA/2J mice. Serum of infected mice also was examined sequentially for alpha/beta interferon (IFN). Despite vigorous lung IFN production, infected mice rarely had detectable circulating IFN. Seemingly, Sendai virus infection can induce transient hyperresponsiveness to a nonviral antigen.
Insights
Sendai virus infection boosts the immune response to sheep red blood cells (RBC) in mice, particularly the IgM and IgG plaque-forming cell (PFC) response. This transient hyperresponsiveness occurs despite low circulating interferon levels.
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- Sendai virus is a common respiratory pathogen.
- Viral infections can modulate the host immune response.
- Understanding immune responses to viral infections is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the effect of Sendai virus infection on the splenic primary plaque-forming cell (PFC) response to sheep red blood cells (RBC).
- To compare the immune response in mouse strains with differing susceptibility to Sendai viral pneumonia.
- To examine the role of interferon (IFN) in this immune modulation.
Main Methods:
- Mice of resistant (C57BL/6J) and susceptible (DBA/2J) strains were inoculated with sheep RBC at varying times relative to Sendai virus infection.
- Splenic PFC responses (IgM, IgG, IgG3, IgG2b) were quantified 6 days post-RBC inoculation.
- Serum and lung samples were analyzed for alpha/beta interferon (IFN) levels.
Main Results:
- Sendai virus infection augmented IgM and IgG-PFC responses in both resistant and susceptible mice.
- Augmentation was most pronounced for IgM, IgG3, and IgG2b PFC.
- Despite significant lung IFN production, circulating IFN levels were rarely detected in infected mice.
Conclusions:
- Sendai virus infection induces a transient hyperresponsiveness to a nonviral antigen (sheep RBC).
- This immune modulation occurs independently of detectable circulating interferon.
- The findings suggest a complex interplay between viral infection and B-cell immunity.