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. 1992 Aug;66(8):5096–5099. doi: 10.1128/jvi.66.8.5096-5099.1992

Rabies virus neuritic paralysis: immunopathogenesis of nonfatal paralytic rabies.

F Weiland 1, J H Cox 1, S Meyer 1, E Dahme 1, M J Reddehase 1
PMCID: PMC241376  PMID: 1629964

Abstract

Two pathogenetically distinct disease manifestations are distinguished in a murine model of primary rabies virus infection with the Evelyn-Rokitnicky-Abelseth strain, rabies virus neuritic paralysis (RVNP) and fatal encephalopathogenic rabies. RVNP develops with high incidence in immunocompetent mice after intraplantar infection as a flaccid paralysis restricted to the infected limb. The histopathologic correlate of this monoplegia is a degeneration of the myelinated motor neurons of the peripheral nerve involved. While, in this model, fatal encephalopathogenic rabies develops only after depletion of the CD4 subset of T lymphocytes and without contribution of the CD8 subset, RVNP is identified as an immunopathological process in which both the CD4 and CD8 subsets of T lymphocytes are critically implicated.

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Selected References

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