We present a review of the clinically oriented literature about BK virus, a relative of JC virus, which is the etiologic agent of progressive multifocal leukoencephalopathy (PML). The kidney, lung, eye, liver, and brain have been proposed as sites of BK virus-associated disease, both primary and reactivated. BK virus has also been detected in tissue specimens from a variety of neoplasms. We believe that BK virus is most often permissively present in sites of disease in immunosuppressed patients, rather than being an etiologic agent that causes symptoms or pathologic findings. There is, however, strong evidence for BK virus-associated hemorrhagic cystitis and nephritis, especially in recipients of solid organ or bone marrow transplants. Now that BK virus can be identified by use of specific and sensitive techniques, careful evaluation of the clinical and pathologic presentations of patients with BK virus will allow us to form a clearer picture of viral-associated pathophysiology in many organ systems.

/pdf/bk-virus-a-clinical-review-1kvf29gtvl.pdf

Bk virus: a clinical review.

BK virus (BKV), a human polyomavirus closely related to JC virus and Simian Virus 40, is ubiquitous in human populations worldwide. After primary infection, BKV establishes a lifelong latent infection in many organs. BKV transforms rodent cells to the neoplastic phenotype and is highly oncogenic in rodents. This review considers the oncogenic potential of BKV in humans and its possible involvement in human tumors. BKV sequences and T antigen (Tag) are detected in several types of human neoplasms, although the viral load is generally low, with less than one copy of the viral genome per cell. The possible causative role of BKV in human oncogenesis rests on the ability of BKV Tag to inactivate the functions of tumor suppressor proteins p53 and pRB family as well as on its ability to induce chromosomal aberrations in human cells. A 'hit and run' mechanism and secretion of paracrine growth factors by BKV Tag-positive cells, recruiting into proliferation neighboring and distant cells, are discussed as possible BKV pathogenic elements in human oncogenesis.

Oncogenic transformation by BK virus and association with human tumors

A total of 480 serum samples from donors including 384 children up to 10 years of age were examined by the hemagglutination-inhibition (HI) test for the rates of prevalence and age of acquisition of HI antibodies against JC virus and BK virus. Among 136 serum samples from various age groups, there were five (4%) with no detectable antibodies against BK or JC virus, 75 (55%) with antibodies against both viruses, 41 (30.1%) with antibodies against only BK virus and 26 (19%) with antibodies against only JC virus. The prevalence of antibodies against JC and BK viruses was 70.5% and 80.8%, respectively, and the mean HI titers (4 x 2n,n greater than or equal to 1) were 4.90 and 4.30. About 50% of the children had acquired antibodies against BK virus by 3 years of age and against JC virus by 6 years of age. These results indicate that dual latent infections with both viruses are common, although independent infections with either virus are predominant in the human population.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1348-0421.1982.tb00254.x

Prevalence Rate and Age of Acquisition of Antibodies against JC Virus and BK Virus in Human Sera

Publisher Summary Several viruses are ubiquitous in the human population and produce a persistent or latent infection in humans. Some of them—such as human polyomaviruses BK (BKV) and JC (JCV)—are oncogenic in experimental systems and are associated with human tumors. This chapter considers the general properties of the human polyomaviruses BK and JC, the characteristics of the latent infection and of the ubiquitous state of these viruses in humans, their transforming capacity in vitro , their oncogenicity in experimental animals, and their possible etiologic role in human tumors are also evaluated. It is noted that the classic Koch's postulates cannot be applied to latent viruses. New rules are considered for these viruses to establish their oncogenic role. It is reported that BKV fulfills these criteria, suggesting that BKV may cooperate, under peculiar conditions, as a cofactor in the development or progression of human tumors. BKV oncogenicity is revealed by cooperating events, such as oncogene activation, loss of tumor suppressor genes, or rearrangements of the viral genome, inducing proliferation of clonal neoplastic cells in a population of latently BKV-infected cells.

BK and JC human polyomaviruses and simian virus 40: natural history of infection in humans, experimental oncogenicity, and association with human tumors.

http://link.springer.com/content/pdf/10.1007/978-1-4613-2221-4_5.pdf

Studies with BK Virus and Monkey Lymphotropic Papovavirus

BK virus (BKV) DNA sequences were not detected in 142 human tumors analyzed by DNA-DNA reassociation kinetics and blot hybridization. The investigation was focused mainly on those rare types of human tumors (ependymomas, choroid plexus papillomas, tumors of pancreatic islets and osteosarcomas) that are induced with highest frequency by BKV in experimental animals. In addition, other tumors of the urinary apparatus and of the central nervous system were analyzed. BKV tumor (T) antigen was not detected in neoplastic tissues, and BKV T antibodies were not found in sera and cerebrospinal fluids from patients with neoplasms. Sequences homologous to BKV DNA were found in normal tissue from a kidney carrying a carcinoma. The neoplastic tissue from the same organ, however, had no sequences homologous to BKV DNA. Such DNA does not belong to BKV but probably to another papovavirus related to BKV.

Lack of Association between BK Virus and Ependymomas, Malignant Tumors of Pancreatic Islets, Osteosarcomas and Other Human Tumors

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Lack of Association between BK Virus and Ependymomas, Malignant Tumors of Pancreatic Islets, Osteosarcomas and Other Human Tumors