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Measles encephalomyelitis--clinical and immunologic studies
Abstract:
We studied 19 patients with postinfectious encephalomyelitis complicating natural measles-virus infections, and our results support the hypothesis that this demyelinating disease has a pathogenesis similar to that of experimental allergic encephalomyelitis. Early myelin destruction was demonstrated by the presence of myelin basic protein in cerebrospinal fluid, and lymphocyte proliferative responses to myelin basic protein were found in 8 of 17 patients tested. A lack of intrathecal synthesis of antibody against measles virus suggests that measles encephalomyelitis may not be dependent on virus replication within the central nervous system. Similar lymphoproliferative responses to myelin basic protein of lymphocytes from single patients with encephalomyelitis after rabies vaccine or after varicella or rubella virus infections suggest a common immune-mediated pathogenesis for the perivenular demyelinating disease that can follow the injection of neural tissues or infection by a variety of viruses.
Insights
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.
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.
- 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.