Meningoencephalitis and demyelination are pathologic manifestations of primary polyomavirus infection in immunosuppressed rhesus monkeys

Michael K. Axthelm, Igor J. Koralnik, Xin Dang, Christian Wüthrich, Daniela Rohne, Isaac E. Stillman, Norman L. Letvin

    Research output: Contribution to journalArticle

    22 Scopus citations

    Abstract

    The human polyomavirus JC (JCV) is the etiologic agent of progressive multifocal leukoencephalopathy (PML), a demyelinating disease of the CNS that occurs in immunosuppressed individuals. Because polyomavirus-induced CNS pathology usually occurs as a result of the reactivation of latent virus, little is known about the disease manifestations of a primary polyomavirus-induced disease in man. To model such a primary infection, SV40-negative rhesus monkeys were immunosuppressed by infection with the virus SHIV-89.6P and then superinfected with the polyomavirus SV40. The animals developed CNS pathology characterized by both demyelination and meningoencephalitis. This observation suggests that a primary polyomavirus infection can be associated with an inflammatory CNS process. These data shed new light on the pathogenic mechanisms of primate polyomaviruses in the immunocompromised host.

    Original languageEnglish (US)
    Pages (from-to)750-758
    Number of pages9
    JournalJournal of Neuropathology and Experimental Neurology
    Volume63
    Issue number7
    DOIs
    StatePublished - Jul 2004

    Keywords

    • Primate model
    • Progressive multifocal leukoencephalopathy (PML)
    • SV40

    ASJC Scopus subject areas

    • Pathology and Forensic Medicine
    • Neurology
    • Clinical Neurology
    • Cellular and Molecular Neuroscience

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