Abstract
The rare demyelinating brain disease, progressive multifocal leukoencephalopathy (PML), was first described by Åström and coworkers (1) in 1958, and a viral etiology was suggested by Zu Rhein and Chou (2) and Silverman and Rubinstein (3) in 1965 based on electron microscopic analysis of infected cells. In 1971, Padgett et al. (4) reported the isolation of a virus from the diseased brain tissue obtained at autopsy from a PML patient. Some have assumed incorrectly that the name given to this virus, JC virus (JCV), identifies it as the agent of Creutzfeldt-Jacob disease, but the name was simply derived from the initials of the PML patient. Structural and antigenic studies (4, 5) demonstrated that JCV was a previously unrecognized member of the genus Polyomavirus within the family Papovaviridae. Additional members of this genus include the closely related human and monkey viruses, BK virus (BKV) and SV40, and the more distantly related type-species, mouse polyomavirus. No evidence has been presented to associate BKV with PML disease. Also, although there have been reports of an SV40 association with human PML (6–11), we believe there is now sufficient evidence to cast doubt on an SV40 etiology for PML and overwhelming data indicating that JCV is the cause of this fatal disease.
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Frisque, R.J., White, F.A. (1992). The Molecular Biology of JC Virus, Causative Agent of Progressive Multifocal Leukoencephalopathy. In: Roos, R.P. (eds) Molecular Neurovirology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-4612-0407-7_2
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