Reappraisal of progressive multifocal leukoencephalopathy due to simian virus 40 |
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Authors: | G L Stoner Caroline F Ryschkewitsch |
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Institution: | (1) Neurotoxicology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 36 Convent Drive, MSC-4126, Bethesda, MD 20892-4126, USA e-mail: stoner@helix.nih.gov, Tel.: 1-301-496-6144, Fax: 1-301-402-1030, US |
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Abstract: | Several cases of progressive multifocal leukoencephalopathy (PML) have been associated with simian virus 40 (SV40), rather
than with JC virus (JCV), the polyomavirus originally isolated from PML tissue. PML has, therefore, been defined as a demyelinating
syndrome with possible multiple viral etiologies. Tissues from three of the cases thought to be associated with SV40 were
available for reexamination. Monoclonal antibodies specific for SV40 capsid antigen VP1, virus-specific biotinylated DNA probes
for in situ hybridization, and virus-specific primers in the polymerase chain reaction (PCR) were used. Macaque PML brain
served as a positive control tissue for SV40 brain infection. Monoclonal antibodies to SV40 VP1 failed to recognize viral
antigen in lesions from all three human PML cases. The biotinylated DNA probe, which reacted with SV40 in macaque PML, failed
to detect SV40 in human PML. However, JCV could be detected by in situ hybridization with a JCV-specific DNA probe. Moreover,
JCV DNA sequences were amplified by PCR from the human PML tissues, whereas SV40 DNA sequences were amplified only from the
macaque brain. Thus, we could not confirm the original reports that the demyelinating agent in these three cases of PML was
SV40, rather than JCV. We conclude that SV40 infection of the central nervous system need not be ruled out in the differential
diagnosis of PML.
Received: 1 December 1997 / Revised, accepted: 23 February 1998 |
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Keywords: | JC virus Demyelination Polyomavirus Central nervous system Macaque |
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