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Viruses can silently prime for and trigger central nervous system autoimmune disease

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Abstract

Although many viruses have been isolated from patients with multiple sclerosis (MS), as yet, no one agent has been demonstrated to cause MS. In contrast, epidemiological data indicate that viral infections are associated with exacerbations of MS. Here, we present data showing that virus infections can subclinically prime animals for central nervous system (CNS) autoimmune disease; long after the original infection has been eradicated, a nonspecific challenge/infection can trigger an exacerbation. The priming infectious agent must show molecular mimicry with self-CNS antigens such as glial fibrillary acidic protein (GFAP), myelin associated glycoprotein (MAG) or myelin proteolipid protein (PLP). The subsequent challenge, however, may be nonspecific; complete Freund’s adjuvant (CFA), or infection with a recombinant vaccinia virus encoding an irrelevant protein, could trigger CNS disease. In the CNS, we could detect a mononuclear cell infiltration, but no demyelination was found. However, if the pathogenesis of MS is similar to that of this novel animal model for CNS autoimmune disease, our findings could help explain why exacerbations of MS are often associated with a variety of different viral infections.

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Authors and Affiliations

  1. Department of Neurology, University of Utah School of Medicine, 30 N 1900 East, RM 3R330, 84132, Salt Lake City, UT, USA

    Diethilde J. Theil, Ikuo Tsunoda & Robert S. Fujinami

  2. Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California, USA

    Fernando Rodriguez & J. Lindsay Whitton

Authors
  1. Diethilde J. Theil
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  2. Ikuo Tsunoda
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  3. Fernando Rodriguez
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  4. J. Lindsay Whitton
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  5. Robert S. Fujinami
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Correspondence to Robert S. Fujinami.

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Theil, D.J., Tsunoda, I., Rodriguez, F. et al. Viruses can silently prime for and trigger central nervous system autoimmune disease. Journal of NeuroVirology 7, 220–227 (2001). https://doi.org/10.1080/13550280152403263

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  • DOI: https://doi.org/10.1080/13550280152403263

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