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Measurement of BK-polyomavirus Non-Coding Control Region Driven Transcriptional Activity Via Flow Cytometry
Published on: July 13, 2019
Detection of JC virus DNA in CSF of pediatric patients with non-PML neurological disorders
Negar Hemmati1, Amir Hossein Alipour1,2, Bahman Abedi Kiasari3
1Department of Microbiology and Immunology, University of Tehran, Tehran, Iran.
Background:
JC virus (JCV) is a human polyomavirus classically associated with progressive multifocal leukoencephalopathy (PML). Its role in other central nervous system (CNS) disorders - and the contribution of related polyomaviruses such as BK virus (BKV) and simian virus 40 (SV40) - remains poorly defined in pediatric populations, especially among immunocompromised patients.
Methods:
We analysed 64 cerebrospinal fluid (CSF) specimens collected from children evaluated for suspected viral encephalitis or meningoencephalitis between March and October 2024. Broad-range and virus-specific PCR assays targeting conserved regions of the large T antigen (LT-ag) and VP1 genes were performed. Positive amplicons were confirmed by bidirectional Sanger sequencing and phylogenetic analysis. Associations with HIV status were assessed using chi-square tests.
Results:
JCV DNA was detected in 4 of 64 samples (4/64; 6.3%), BKV DNA in 5 of 64 samples (5/64; 7.8%), and both viruses were co-detected in 3 samples (3/64; 4.7%). All positive detections occurred in HIV-positive patients (JCV: 4/19 HIV+; BKV: 5/19 HIV+), yielding statistically significant associations with HIV status (JCV p = 0.006; BKV p = 0.002). No SV40 DNA was identified. Phylogenetic reconstruction grouped patient sequences tightly with reference JCV and BKV strains, supporting authentic detection rather than laboratory contamination.
Conclusions:
These results provide molecular evidence that JCV and BKV can be detected in the CSF of pediatric patients with suspected CNS infection - predominantly in the setting of HIV-associated immunosuppression - and may represent underrecognized contributors to non-PML neurological disease. Larger, longitudinal studies integrating clinical, radiological and quantitative viral-load data are required to define causality and clinical impact.
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