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Immunostimulation in mice infected with Sendai virus.

D G Brownstein1, E C Weir

  • 1Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06510.

American Journal of Veterinary Research
|December 1, 1987
PubMed
Summary

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.

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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.

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  • 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.