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Measles virus spread and pathogenesis in genetically modified mice

B Mrkic1, J Pavlovic, T Rülicke

  • 1Institut für Molekularbiologie Abt. I, Universität Zürich, Zürich, Switzerland.

Journal of Virology
|August 8, 1998
PubMed
Summary

Alpha/beta interferon in mice controls measles virus (MV-Edm) infection. A high-affinity receptor aids MV spread and pathogenesis, but is not essential.

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Area of Science:

  • Virology
  • Immunology
  • Genetics

Background:

  • Attenuated Edmonston measles virus (MV-Edm) typically shows limited pathogenicity in standard mice.
  • Understanding measles virus (MV) pathogenesis requires models that mimic human susceptibility.
  • Interferon signaling and receptor interactions are critical in viral control.

Purpose of the Study:

  • To investigate the role of alpha/beta interferon in controlling MV infection in mice.
  • To examine the impact of a high-affinity receptor (human CD46) on MV spread and pathogenesis.
  • To establish a mouse model for studying MV encephalitis.

Main Methods:

  • Infection of mice with targeted mutations in the alpha/beta interferon receptor.
  • Generation of genetically modified mice expressing human CD46 with human-like tissue specificity.

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  • Intranasal and intracerebral inoculation of MV-Edm in different mouse models.
  • Assessment of virus propagation, inflammatory responses, and clinical outcomes.

    • Main Results:

    • MV-Edm showed limited lung propagation in mice lacking alpha/beta interferon receptors.
    • Intracerebral MV-Edm inoculation was lethal in approximately half of these mice.
    • Mice expressing human CD46 and lacking alpha/beta interferon exhibited enhanced MV spread to lungs, PBMCs, spleen, and liver.
    • Intracerebral MV-Edm infection in these modified mice led to encephalitis with a high mortality rate.

    Conclusions:

    • Alpha/beta interferon signaling is a key determinant of MV infection control in mice.
    • A high-affinity receptor facilitates MV spread and pathogenesis but is not strictly required.
    • The developed mouse model is valuable for studying MV encephalitis and viral pathogenesis.