Abstract
After more than a decade of clinical descriptions of a human demyelinating disease known as progressive multifocal leukoencephalopathy (PML),1–3 a virus was finally isolated from affected brain tissue by Padgett et al.4 in 1971. Named JC virus after the initials of the patient, the agent quickly became grouped in the family of Papovavirus on the basis of the viral architecture, size, and genome content. Concurrently, another human papovavirus was isolated by Gardner and her colleagues5 from the urine of a renal transplant recipient and also named after the initials of the patient, BK. Although BK virus (BKV) is still not clearly identified with a specific disease, JC virus (JCV) is now recognized as the causative agent for PML and has been repeatedly isolated from demyelinated brain tissue of suspected PML patients. In order to identify the different isolates made from human brain tissue,6 the designation of the location of the isolation (in Madison, Wisconsin) and a serial number of the isolate were used, e.g., Mad-1 the prototype; Mad-4. The long delay from suspicion of a viral etiology to the final viral isolation was caused largely by the host restriction for growth of JCV in cell culture. The successful isolation made by Padgett et al. required the use of human fetal brain cells and several months in culture. Such cultures are composed of macroglial cells and their precursors, which become the target cells for infection in the adult and undergo demyelination. Neurotropism is one of the chief characteristics of JCV and is the singular feature of this viral pathogen that has generated the most experimental attention.
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Major, E.O., Vacante, D.A., Houff, S.A. (1992). Human Papovaviruses. In: Specter, S., Bendinelli, M., Friedman, H. (eds) Neuropathogenic Viruses and Immunity. Infectious Agents and Pathogenesis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5886-2_11
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