BK Polyomavirus—Biology, Genomic Variation and Diagnosis

Abstract

The BK polyomavirus (BKPyV), a representative of the family Polyomaviridae, is widespread in the human population. While the virus does not cause significant clinical symptoms in immunocompetent individuals, it is activated in cases of immune deficiency, both pharmacological and pathological. Infection with the BKPyV is of particular importance in recipients of kidney transplants or HSC transplantation, in which it can lead to the loss of the transplanted kidney or to haemorrhagic cystitis, respectively. Four main genotypes of the virus are distinguished on the basis of molecular differentiation. The most common genotype worldwide is genotype I, with a frequency of about 80%, followed by genotype IV (about 15%), while genotypes II and III are isolated only sporadically. The distribution of the molecular variants of the virus is associated with the region of origin. BKPyV subtype Ia is most common in Africa, Ib-1 in Southeast Asia, and Ib-2 in Europe, while Ic is the most common variant in Northeast Asia. The development of molecular methods has enabled significant improvement not only in BKPyV diagnostics, but in monitoring the effectiveness of treatment as well. Amplification of viral DNA from urine by PCR (Polymerase Chain Reaction) and qPCR Quantitative Polymerase Chain Reaction) is a non-invasive method that can be used to confirm the presence of the genetic material of the virus and to determine the viral load. Sequencing techniques together with bioinformatics tools and databases can be used to determine variants of the virus, analyse their circulation in populations, identify relationships between them, and investigate the directions of evolution of the virus.

Molecular Epidemiology and Variation of the BK Polyomavirus in the Population of Central and Eastern Europe Based on the Example of Poland

“…Reactivation of infection is initially asymptomatic, with asymptomatic viruria followed by viraemia when viral particles enter the bloodstream [8]. In such patients, reactivation of the virus or its acquisition via transplant can cause a number of serious complications, including BK polyomavirus-associated nephropathy (BKPyVAN), leading to loss of the graft following a kidney transplant or severe haemorrhagic cystitis (HC) following an allogeneic haematopoietic stem-cell transplant (HSCT) [5,[9][10][11][12][13]. For this reason, the presence and rate of replication of BKPyV should be monitored in recipients.…”

Genetic polymorphisms in TLR3, IL10 and CD209 influence the risk of BK polyomavirus infection after kidney transplantation

“…BK polyomavirus (BKPyV) is a double-stranded DNA virus belonging to the Polyomaviridae family 11 . Primary infection occurs during early childhood and is usually asymptomatic, whereas seroprevalence rates exceed 90% in the adult population 12 , 13 . The reactivation of latent BKPyV infection may result in the development of BKPyV-associated nephropathy (BKPyVAN), a major cause of graft loss after kidney transplantation (KT) 14 , 15 .…”

Genotypes and Variants of BKPyV in Organ Donors after Brain Death

“…The first classification of BKPyV into genotypes was described in 1993 by Jin et al [ 35 ] who detected the restriction sites specific for a given genotype in the variable region of the gene encoding the VP1 protein, which were detected by restriction fragment length polymorphism (RFLP). Nowadays, genotyping of the BKPyV is mostly based on the sequencing of the polymorphic fragment of BC loop (VP1 protein) which contains the region with nucleotides at positions 1744–1812 used for identification of the four main BKPyV genotypes [ 36 , 37 ]. Sanger sequencing is still used successfully for BKPyV genotyping due to the relatively short length of the sequence used to classify the virus into subtypes [ 38 , 39 ].…”