Glial brain tumours with their poor prognosis, limited treatment modalities and unclear detailed pathophysiology represent a significant health concern. The purpose of the current study was to investigate and describe the possible role of the human polyomavirus JC as an underlying cancerogenic or co-cancerogenic factor in the complex processes of glial tumour induction and development. Samples from 101 patients with glial tumours were obtained during neurosurgical tumour resection. Small tissue pieces were taken from several areas of the histologically verified solid tumour core. Biopsies were used for DNA extraction and subsequent amplification reactions of sequences from the JC viral genome. Real-time polymerase chain reaction was used for detection and quantification of its non-coding control region (NCCR) and gene encoding the regulatory protein Large T antigen (LT). An average of 37.6% of all patients was found to be LT positive, whereas only 6.9% tested positive for NCCR. The analysis of the results demonstrated significant variance between the determined LT prevalence and the rate for NCCR, with a low starting copy number in all positive samples and threshold cycles in the range of 36 to 42 representing viral load in the range from 10 to 1000 copies/μl. The results most probably indicate incomplete JC viral replication. Under such conditions, mutations in the host cell genome may be accumulated due to interference of the virus with the host cell machinery, and eventually malignant transformation may occur.
Polyomavirus hominis 1 (BK virus, BKV) is an important pathogen in the field of transplantation medicine. BKV reactivation among renal-transplant recipients could cause BK associated nephropathy, which has unfavorable prognosis and is a cause for graft rejection. It is not clear why only few transplanted patients develop BK associated nephropathy while most exhibit asymptomatic viruria. One of the possible reasons lies in the mutations of the VP1 gene, encoding the main structural protein, bearing important determinants for the recognition of specific cellular receptors. The change of amino acid sequence could result in altered pathogenicity of BKV. The amplified sequences of BK in this research were from urines of patients with various clinical conditions along with healthy individuals. Nevertheless the sequence analysis which was undertaken did not show correlation between the viral genotype and the clinical condition. It was demonstrated that the most common BKV genotype in Bulgaria is genotype I and that the strains common in Bulgaria (genotypes I and IV) have typical European origin. Most of the sequenced BKV DNA samples (8/10) were correlated with the highest degree of similarity (81%) to the subcluster Ib. A specific place among the samples is taken by Pr-9, amplified from the urine of a pregnant woman that has a different evolutionary origins and might establish the beginning of a new distinct BKV strain.
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