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 journalArticlepeer-review

25 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

  • General Medicine

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