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Rearrangement patterns of JC virus noncoding control region from different biological samples
V Pietropaolo1, M Videtta, D Fioriti
1Department of Public Health Sciences, University of Rome "La Sapienza," Rome, Italy. Pietropaolo@uniroma1.it
Journal of Neurovirology
|November 7, 2003
Summary
JC virus (JCV) causes progressive multifocal leukoencephalopathy (PML), especially in AIDS patients. JCV NCCR rearrangements in PBMCs and CSF, unlike urine, may promote PML development.
Area of Science:
- Neurovirology
- Molecular Virology
Background:
- JC virus (JCV) is the causative agent of progressive multifocal leukoencephalopathy (PML), a severe demyelinating brain disease.
- PML predominantly affects immunosuppressed individuals, notably those with acquired immunodeficiency syndrome (AIDS).
- JCV establishes latent infection in kidneys, with potential for reactivation and genetic variation.
Purpose of the Study:
- To investigate the genetic variability of the JCV noncoding control region (NCCR) in different biological samples.
- To analyze the structural rearrangements of the JCV NCCR and their potential correlation with PML pathogenesis.
- To compare JCV NCCR sequences from urine, PBMCs, and CSF with the archetype strain.
Main Methods:
- Polymerase chain reaction (PCR) was employed to detect the JCV genome in urine, PBMCs, and CSF.
- Sequencing of PCR-amplified fragments allowed for NCCR structure analysis.
- Homology and multiple alignment analyses were performed to compare isolated JCV strains with the archetype.
Main Results:
- JCV DNA was detected in urine, PBMCs, and CSF samples.
- NCCR sequences from urine samples closely resembled the archetype strain.
- PBMCs and CSF samples exhibited distinct and characteristic NCCR rearrangements compared to the archetype.
Conclusions:
- JCV NCCR sequences display significant variability depending on the biological compartment.
- Specific NCCR rearrangements found in PBMCs and CSF may indicate adaptation for PML development.
- Further research is warranted to elucidate the precise role of these rearrangements in PML pathogenesis.