TY - JOUR
T1 - JC virus load in cerebrospinal fluid and transcriptional control region rearrangements may predict the clinical course of progressive multifocal leukoencephalopathy
AU - Delbue, Serena
AU - Elia, Francesca
AU - Carloni, Camilla
AU - Tavazzi, Eleonora
AU - Marchioni, Enrico
AU - Carluccio, Silvia
AU - Signorini, Lucia
AU - Novati, Stefano
AU - Maserati, Renato
AU - Ferrante, Pasquale
PY - 2012/10
Y1 - 2012/10
N2 - Progressive multifocal leukoencephalopathy (PML) is a severe disease of the central nervous system (CNS), caused by infection with the Polyomavirus JC virus (JCV). Because there are no known treatments or prognostic factors, we performed a long-term study focusing mainly on cerebrospinal fluid (CSF) samples from PML patients to describe the virological features akin to the different forms of the disease. Twenty-eight PML patients were enrolled: 10 HIV-1+ patients with classical PML (CPML), 9 HIV-1+ patients with slowly progressing or stable neurological symptoms (benign PML), 3 HIV-1+ asymptomatic patients, and 6 HIV-1-negative patients. CSF, urine, and blood samples were collected at the enrollment (baseline) and every 6 months afterwards when possible. The JCV DNA and HIV-1 RNA loads were determined, and the JCV strains were characterized. At baseline, the mean CSF JCV load was log6.0±1.2copies/ml for CPML patients, log4.0±1.0 copies/ml for benign PML patients, log4.2±0.5 copies/ml for asymptomatic PML patients, and log5.8±1.3copies/ml for HIV-1-negative PML patients (CPML vs. benign: P
AB - Progressive multifocal leukoencephalopathy (PML) is a severe disease of the central nervous system (CNS), caused by infection with the Polyomavirus JC virus (JCV). Because there are no known treatments or prognostic factors, we performed a long-term study focusing mainly on cerebrospinal fluid (CSF) samples from PML patients to describe the virological features akin to the different forms of the disease. Twenty-eight PML patients were enrolled: 10 HIV-1+ patients with classical PML (CPML), 9 HIV-1+ patients with slowly progressing or stable neurological symptoms (benign PML), 3 HIV-1+ asymptomatic patients, and 6 HIV-1-negative patients. CSF, urine, and blood samples were collected at the enrollment (baseline) and every 6 months afterwards when possible. The JCV DNA and HIV-1 RNA loads were determined, and the JCV strains were characterized. At baseline, the mean CSF JCV load was log6.0±1.2copies/ml for CPML patients, log4.0±1.0 copies/ml for benign PML patients, log4.2±0.5 copies/ml for asymptomatic PML patients, and log5.8±1.3copies/ml for HIV-1-negative PML patients (CPML vs. benign: P
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U2 - 10.1002/jcp.24051
DO - 10.1002/jcp.24051
M3 - Article
C2 - 22253012
AN - SCOPUS:84862658163
VL - 227
SP - 3511
EP - 3517
JO - Journal of cellular and comparative physiology
JF - Journal of cellular and comparative physiology
SN - 0021-9541
IS - 10
ER -