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1 Institute of Virology and Immunobiology, University of Würzburg, Versbacher Straße 7, D-97078 Würzburg, Germany
2 Institute of Neurology, Schwarzspanierstraße 17, A-1090 Vienna, Austria
and3 Federal Research Centre for Virus Diseases of Animals, Friedrich Loeffler Institutes, D-17498 Insel Riems, Germany
The neurotropic mouse hepatitis virus MHV-JHM induces central nervous system (CNS) demyelination in Lewis rats that pathologically resembles CNS lesions in multiple sclerosis. The mechanisms of MHV-JHM-induced demyelination remain unclear and several studies have implicated the role of the immune response in this process. We have shown previously that protective immunity against MHV-JHM-induced encephalomyelitis was induced by immunization with a vaccinia virus (VV) recombinant expressing MHV-JHM S-protein (VV-S). Here, we present evidence that the time of MHV-JHM challenge after immunization with VV-S plays a critical role in protective immunity. The induction of virus-neutralizing S-protein-specific antibodies prior to the MHV-JHM challenge modulates the disease process and a subacute encephalomyelitis based on a persistent virus infection developed. Typical pathological alterations were lesions of inflammatory demyelination. In addition, the results indicate that after seroconversion, CD8+ T cells were no longer essential for virus elimination in contrast to their role in protection during acute encephalomyelitis.
* Author for correspondence. Fax +49 38351 7151.
Received 5 September 1994;
accepted 1 December 1994.
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