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Theiler's virus infection: a model for multiple sclerosis
Journal article   Open access   Peer reviewed

Theiler's virus infection: a model for multiple sclerosis

Emilia L Oleszak, J Robert Chang, Herman Friedman, Christos D Katsetos and Chris D Platsoucas
Clinical microbiology reviews, v 17(1)
Jan 2004
PMID: 14726460
url
https://doi.org/10.1128/cmr.17.1.174-207.2004View
Published, Version of Record (VoR)Open Access (License Unspecified) Open

Abstract

Animals Cardiovirus Infections - immunology Cardiovirus Infections - metabolism Cardiovirus Infections - physiopathology Disease Models, Animal Humans Models, Immunological Multiple Sclerosis - immunology Multiple Sclerosis - metabolism Multiple Sclerosis - physiopathology Theilovirus - pathogenicity
Both genetic background and environmental factors, very probably viruses, appear to play a role in the etiology of multiple sclerosis (MS). Lessons from viral experimental models suggest that many different viruses may trigger inflammatory demyelinating diseases resembling MS. Theiler's virus, a picornavirus, induces in susceptible strains of mice early acute disease resembling encephalomyelitis followed by late chronic demyelinating disease, which is one of the best, if not the best, animal model for MS. During early acute disease the virus replicates in gray matter of the central nervous system but is eliminated to very low titers 2 weeks postinfection. Late chronic demyelinating disease becomes clinically apparent approximately 2 weeks later and is characterized by extensive demyelinating lesions and mononuclear cell infiltrates, progressive spinal cord atrophy, and axonal loss. Myelin damage is immunologically mediated, but it is not clear whether it is due to molecular mimicry or epitope spreading. Cytokines, nitric oxide/reactive nitrogen species, and costimulatory molecules are involved in the pathogenesis of both diseases. Close similarities between Theiler's virus-induced demyelinating disease in mice and MS in humans, include the following: major histocompatibility complex-dependent susceptibility; substantial similarities in neuropathology, including axonal damage and remyelination; and paucity of T-cell apoptosis in demyelinating disease. Both diseases are immunologically mediated. These common features emphasize the close similarities of Theiler's virus-induced demyelinating disease in mice and MS in humans.

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Collaboration types
Domestic collaboration
Web of Science research areas
Microbiology
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