Abstract
The human polyomavirus, JCV, is the etiological agent of a fatal central nervous system (CNS) demyelinating disease known as progressive multifocal leukoencephalopathy, or PML. Seroepidemiological studies have indicated that greater than 70% of the human population worldwide is infected with JCV. Like other polyomaviruses, JCV establishes a lifelong latent or persistent infection in its natural host (1–5). Reactivation of JCV in the setting of an underlying immunosuppressive illness, such as AIDS, leads to virus dissemination to the CNS, infection of oligodendrocytes, and the development of PML (1,2,6,7). Not surprisingly, the incidence of PML has increased dramatically as a result of the AIDS pandemic. A recent epidemiological study has found that PML increased twentyfold from 0.2 cases per million people in 1979 to 3.3 cases per million people in 1994 (8). The increase in PML has renewed an interest in studying the biology of this common human polyomavirus.
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References
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© 2001 Humana Press Inc., Totowa, NJ
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Liu, C.K., Atwood, W.J. (2001). Propagation and Assay of the JC Virus. In: Raptis, L. (eds) SV40 Protocols. Methods in Molecular Biology™, vol 165. Humana Press. https://doi.org/10.1385/1-59259-117-5:9
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DOI: https://doi.org/10.1385/1-59259-117-5:9
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