Experimental Measles Encephalomyelitis in the Rat: Generation of Measles Virus (MV) and T-Lymphocyte Cell Lines Specific for Myelin Basic Protein (MBP)

  • U. G. Liebert
  • C. Linington
  • V. ter Meulen
Part of the Verhandlungen der Deutschen Gesellschaft für Neurologie book series (VDGNEUROLOGIE, volume 4)


The pathogenetic mechanisms involved in human measles encephalitits are poorly understood. Circumstantial evidence suggests an autoimmune pathogenesis for measles encephalitis in man (3,4). In order to analyse this aspect, an experimental model has been established in the Lewis rat, an animal species in which autoimmune reactions can be induced (2,8). A subacute measles encephalomyelitis (SAME) occurs after intracerebral inoculation with measles virus (MV) (5). The disease is char-acterized clinically by seizures, weight loss, unsteadiness, various degrees of paresis, and neuropathologically by prominent lymphomonocytic perivascular infiltration of the grey and white matter of the entire central nervous System (CNS) with resemblance to experimental allergic encephalitis, but demyelination is not apparent. Infectious measles virus cannot be recovered from animals with SAME. Molecular characterization of the measles virus persistence in brain cells of SAME rats has indicated restriction of the expression of the measlesvirus-envelope genes, as in subacute sclerosing panencephalitis (1). After recovery from clinical disease, animals reveal histologically either persisting inflammatory lesions or residual changes indicative of a preceding encephalitis.


  1. 1.
    Baczko K, Liebert UG, et al. (1986) Expression of defective measles virus genes in brain tissues of patients with subacute sclerosing panencephalitis. J Virol 59:472–478PubMedGoogle Scholar
  2. 2.
    Gasser DL, et al. (1973) Genetic control of susceptibility to experimental allergic encephalitis in rats. Science 181:872–873PubMedCrossRefGoogle Scholar
  3. 3.
    Gendelman HE, et al. (1984) Measles encephalorayelitis: Lack of evidence of viral invasion of the central nervous System and quantitative studies of the nature of demyelination. Ann Neurol 15:353–360PubMedCrossRefGoogle Scholar
  4. 4.
    Johnson RT, et al. (1984) Measles encephalomyelitis: Clinical and immunologcial studies. N Engl J Med 310:137–141PubMedCrossRefGoogle Scholar
  5. 5.
    Liebert UG, ter Meulen V (1986) Measles virus induced encephalomyelitis in Lewis and BN rats. J Gen Virol (in press)Google Scholar
  6. 6.
    Liebert UG, Linington C, ter Meulen V (1986) Induction of autoimmune reactions to myelin basic protein in measles virus infected Lewis rats. (submitted)Google Scholar
  7. 7.
    Linington C, et al. (1984) A permanent rat T cell line that mediates experimental allergic neuritis in the Lewis rat in vivo. J Immunol 133:1946–1950PubMedGoogle Scholar
  8. 8.
    Watanabe R, Wege H, ter Meulen V (1983) Adoptive transfer of EAE-like lesions from rats with coronavirus-induced demyelinating encephalomyelitis. Nature 305:150–153PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1987

Authors and Affiliations

  • U. G. Liebert
  • C. Linington
  • V. ter Meulen

There are no affiliations available

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