PML, a fatal disease of human brain characterized by many disseminated regions of demyelination, is generally considered to be caused by the polyomavirus JC virus (JCV). In contrast the etiology of MS, which is characterized by plaques representing discrete sclerotic demyelmated regions, remains unknown although several viruses have been proposed to trigger an autoimmune process of oligodendrocyte death. Using a powerful two-step procedure for in-situ polymerase chain reaction (ISPCR) to amplify and detect viral gene sequences in archival sections of human brain tissue, we have gathered preliminary data showing a high prevalence of HHV6 in both PML and MS white matter, but not in similar tissues from control cases including Parkinson's, glioblastoma, AIDS and fetal brain. In 4/4 cases of PML there were 50-100 HHV6 infected cells per 20X field in heavily involved regions, and 20-50 concentrated in periplaque regions in 3/5 cases of MS. In contrast, there were generally fewer than 5 infected cells per 20X field even in the most pathologic regions of controls included in the same experimental run. By morphological criteria, predominantly oligodendrocytes and mononuclear cells were infected. These data support a role for HHV6 in the pathogenesis of both MS and PML, and suggest that immune factors may account for the neuropathological differences.
|Original language||English (US)|
|Number of pages||1|
|Journal||Clinical Infectious Diseases|
|State||Published - Dec 1 1997|
ASJC Scopus subject areas
- Microbiology (medical)
- Infectious Diseases