Analysis of the transcriptional control region of JC polyomavirus in cerebrospinal fluid from HIV-negative patients with progressive multifocal leucoencephalopathy

2006 ◽  
Vol 78 (10) ◽  
pp. 1271-1275 ◽  
Author(s):  
Cesare Giovanni Fedele ◽  
Carolina Polo ◽  
Antonio Tenorio ◽  
Jordi Niubò ◽  
Maria Rosa Ciardi ◽  
...  
Virology ◽  
2008 ◽  
Vol 380 (1) ◽  
pp. 118-123 ◽  
Author(s):  
Yoshiaki Yogo ◽  
Shan Zhong ◽  
Ayako Shibuya ◽  
Tadaichi Kitamura ◽  
Yukio Homma

2015 ◽  
Vol 69 (3) ◽  
pp. 417-434
Author(s):  
Tetsuo Takahashi ◽  
Takashi Nedachi ◽  
Takuya Etoh ◽  
Hiroyuki Tachikawa ◽  
Xiao-Dong Gao

2001 ◽  
Vol 82 (4) ◽  
pp. 899-907 ◽  
Author(s):  
Monica Sala ◽  
Jean-Pierre Vartanian ◽  
Pascale Kousignian ◽  
Jean-François Delfraissy ◽  
Yassine Taoufik ◽  
...  

Progressive multifocal leukoencephalopathy (PML) is a rapidly fatal demyelinating disease of the central nervous system related to JC polyomavirus (JCV) replication in oligodendrocytes. PML usually occurs in immunocompromised individuals, especially in the setting of AIDS. Administration of highly active anti-retroviral therapy (HAART) may improve survival prognosis in some, but not all, patients with AIDS-related PML. This observation might be explained by the outgrowth of some JCV variants of increased fitness. To evaluate this hypothesis, two subgroups of five patients with AIDS-related PML, started on HAART after PML diagnosis, were analysed. The non-responder (NR) patients died rapidly despite HAART, while responders (R) had a positive outcome and were still alive. JCV DNA was extracted from cerebrospinal fluid biopsies and two regions of the genome were analysed, the transcriptional control region (TCR) and the major capsid protein gene (VP1). Both regions show different degrees of polymorphism and are recognized as evolving independently. Sequence analysis demonstrated that (i) extensive TCR rearrangements were present in both subgroups of patients, (ii) VP1 sequence polymorphisms could be identified in the BC loop, suggesting the absence of immune selection, and (iii) no genomic marker for JCV specific neurovirulence could be identified in the TCR and VP1 loci.


FEBS Letters ◽  
1990 ◽  
Vol 271 (1-2) ◽  
pp. 33-36 ◽  
Author(s):  
S. Mosselman ◽  
J.W.M. Höppener ◽  
L. de Wit ◽  
W. Soeller ◽  
C.J.M. Lips ◽  
...  

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