{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T14:17:53Z","timestamp":1790864273847,"version":"4.1.0"},"reference-count":41,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2006,8,22]],"date-time":"2006-08-22T00:00:00Z","timestamp":1156204800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Medical Virology"],"published-print":{"date-parts":[[2006,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The human polyomavirus JC (JCV) is the causative agent of progressive multifocal leukoencephalopathy (PML), a fatal demyelinating disease of the central nervous system (CNS). JCV has a hyper\u2010variable non\u2010coding transcriptional control region (TCR), which contains the origin of replication and the promoters of viral transcription and replication. The archetype form of TCR\u2010JCV is frequently found in the urine and kidneys of healthy and immunocompromised subjects. However, the rearranged forms, possibly generated by deletion and duplication of segments of the archetype sequence, are found in the peripheral blood, cerebrospinal fluid (CSF), and brain of PML patients. Most experience on this setting has come from the human immunodeficiency virus (HIV) pandemic. Little has been described on the JCV\u2010TCR sequences from PML\u2010HIV\u2010negative patients affected by other immunosuppressive disorders. The aim of this study was to analyze the JCV\u2010TCR detected in CSF samples from 12 HIV\u2010negative immunosuppressed patients suffering from PML and to investigate the possible role of genomic organization in the different incidences of PML in HIV\u2010positive and HIV\u2010negative patients. The results confirm that the JCV\u2010TCR rearrangements play a crucial role in the development of PML, although they do not account for the higher frequency of the disease in HIV infection. These data support the hypothesis that, independently of the rearrangement patterns of JCV\u2010TCR, the direct action of HIV together with other as yet unidentified cellular determinants can be a key to explaining the high rate of PML in HIV infection with respect to other underlying immunosuppressive conditions. J. Med. Virol. 78:1271\u20131275, 2006. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jmv.20697","type":"journal-article","created":{"date-parts":[[2006,8,22]],"date-time":"2006-08-22T23:23:14Z","timestamp":1156288994000},"page":"1271-1275","source":"Crossref","is-referenced-by-count":4,"title":["Analysis of the transcriptional control region of JC polyomavirus in cerebrospinal fluid from HIV\u2010negative patients with progressive multifocal leucoencephalopathy"],"prefix":"10.1002","volume":"78","author":[{"given":"Cesare 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