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Related Experiment Videos

Measles encephalomyelitis--clinical and immunologic studies.

R T Johnson, D E Griffin, R L Hirsch

    The New England Journal of Medicine
    |January 19, 1984
    PubMed
    Summary

    This study suggests postinfectious encephalomyelitis, a demyelinating disease, shares a similar immune-mediated pathogenesis with experimental allergic encephalomyelitis. Measles virus infection may trigger this through myelin basic protein, not direct viral replication in the central nervous system.

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    Area of Science:

    • Neuroimmunology
    • Demyelinating Diseases
    • Viral Encephalomyelitis

    Background:

    • Postinfectious encephalomyelitis (PIE) is a rare neurological complication following viral infections.
    • The pathogenesis of PIE, particularly following measles virus infection, remains incompletely understood.
    • Experimental allergic encephalomyelitis (EAE) serves as a model for immune-mediated demyelinating diseases.

    Purpose of the Study:

    • To investigate the pathogenesis of measles virus-induced encephalomyelitis.
    • To explore the role of myelin basic protein (MBP) and immune responses in PIE.
    • To compare the pathogenesis of measles PIE with EAE and other post-vaccination/viral encephalitides.

    Main Methods:

    • Analysis of cerebrospinal fluid (CSF) for myelin basic protein (MBP) in 19 patients with measles PIE.

    Related Experiment Videos

  • Assessment of lymphocyte proliferative responses to MBP in 17 patients.
  • Evaluation of intrathecal antibody synthesis against measles virus.

    • Main Results:

    • Evidence of early myelin destruction was found via MBP in CSF.
    • Lymphocyte proliferation in response to MBP was observed in 8 of 17 patients.
    • Lack of intrathecal antibody synthesis against measles virus suggested limited CNS viral replication.

    Conclusions:

    • Measles virus-induced encephalomyelitis likely shares an immune-mediated pathogenesis with EAE.
    • The disease appears to be triggered by immune responses to myelin components, not direct viral CNS infection.
    • A common immune-mediated pathogenesis is suggested for perivenular demyelinating diseases following various viral infections or neural tissue vaccinations.