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Progressive Multifocal Leukoencephalopathy: Molecular Biology, Pathogenesis and Clinical Impact

 

作者: Thomas Weber,   Eugene O. Major,  

 

期刊: Intervirology  (Karger Available online 1997)
卷期: Volume 40, issue 2-3  

页码: 98-111

 

ISSN:0300-5526

 

年代: 1997

 

DOI:10.1159/000150537

 

出版商: S. Karger AG

 

关键词: Polyomaviruses;Tumor biology;Progressive multifocal leukoencephalopathy

 

数据来源: Karger

 

摘要:

The human polyomaviruses JC virus (JCV) and BK virus (BKV) have long been known as onco- and neurooncogenic. Interest in their oncogenic potential has reemerged with the discovery of simian virus 40 DNA in human brain tumors including the pituitary as well as in bone tumors and mesotheliomas. The only human disease caused by an infection with the human polyomavirus JCV is progressive multifocal leukoencephalopathy (PML) characterized by a lytic infection of oligodendrocytes with consecutive demyelination. Malignant transformation of cell lines appears to be caused by a complex interaction of the viral large T (tumor) antigen with several transcription factors and tumor suppressor proteins such as p53 and the retinoblastoma protein. PML, once an extremely rare disease, has become much more frequent in the western world owing to the AIDS pandemic. An exceedingly complicated, cell-, tissue- and species-specific pattern of protein-DNA interaction and negative as well as positive feedback regulation by at least a dozen proteins and possibly mutations in the JC viral promoter-enhancer region govern host range and development of PML. The intricate molecular and immunological prerequisites ultimately leading to PML in humans have not yet been completely elucidated.

 

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