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Journal of Infection and Public Health Jun 2011
Topics: BK Virus; Central Nervous System Infections; Humans; Polyomavirus Infections; Tumor Virus Infections; Viral Tropism
PubMed: 21663880
DOI: 10.1016/j.jiph.2011.02.002 -
Seminars in Cancer Biology Aug 2009BK virus (BKV) is a polyomavirus that ubiquitously infects the human population. Following a typically subclinical primary infection, BKV establishes a life-long... (Review)
Review
BK virus (BKV) is a polyomavirus that ubiquitously infects the human population. Following a typically subclinical primary infection, BKV establishes a life-long persistent infection in the kidney and urinary tract. BKV is known to reactivate and cause severe disease in immunosuppressed patients, particularly renal and bone marrow transplant patients. Infection of BKV in rodent animal models or cells in culture often results in tumor formation or transformation, respectively. When co-expressed with activated oncogenes, BKV large tumor antigen drives the transformation of primary human cells. An etiological role of BKV in human cancer, however, remains controversial. Multiple reports have demonstrated conflicting results in regards to the presence of BKV sequences and/or proteins in various tumor types. This review compiles the most recent findings of BKV detection in a number of human cancers. Due to the lack of conclusive causality data from these studies, there does not appear to be a definitive association between BKV and human cancers.
Topics: Animals; BK Virus; Humans; Neoplasms; Polyomavirus Infections; Tumor Virus Infections
PubMed: 19505653
DOI: 10.1016/j.semcancer.2009.02.004 -
Ophthalmology Dec 1999
Topics: AIDS-Related Opportunistic Infections; BK Virus; Eye Infections, Viral; Humans; Papillomavirus Infections; Retinitis; Tumor Virus Infections
PubMed: 10599646
DOI: 10.1016/S0161-6420(99)90566-3 -
Annals of Transplantation 2012The increasing prevalence of BK virus nephropathy (BKVN) observed in recent years, with its consequent impact on kidney allograft survival rates, has focused attention... (Review)
Review
The increasing prevalence of BK virus nephropathy (BKVN) observed in recent years, with its consequent impact on kidney allograft survival rates, has focused attention on the relationship between immunosuppression regimens and risk of BK virus reactivation. The adoption of more potent immunosuppressive regimens over the last two decades, notably tacrolimus with mycophenolic acid and corticosteroids, appears to be associated with higher rates of BK activation. There is also evidence of a specific increase in risk for tacrolimus-based immunosuppression vs. cyclosporine, which in vitro data suggest may be at least partly due to differences in antiviral activity. Early concerns that mammalian target of rapamycin (mTOR) inhibitor use was associated with development of BKVN do not appear to have been borne out. Protocol-driven BK virus screening is recommended to facilitate early diagnosis and intervention, which primarily comprises the controlled reduction or discontinuation of immunosuppressive drugs. Although a consensus on the optimal strategy for immunosuppression modification is still lacking, early diagnosis of BK reactivation and pre-emptive modification of immunosuppression has resulted in a marked improvement in graft outcomes. Typically, intervention consists of reducing calcineurin inhibitor exposure before or after antimetabolite dose reduction, withdrawal of one agent from a triple therapy regimen, or switching between agents within a therapeutic class. A benefit for antiviral therapy is not yet confirmed. While more data are required, the current evidence base is adequate to justify routine screening with early modification of the intensity and nature of the immunosuppression regimen to reduce the toll of BKVN in the kidney transplant population.
Topics: BK Virus; Cyclosporine; Humans; Immunosuppressive Agents; Kidney Diseases; Kidney Transplantation; Polyomavirus Infections; Risk Factors; Tacrolimus; Tumor Virus Infections; Virus Replication
PubMed: 22466913
DOI: 10.12659/aot.882640 -
Advances in Experimental Medicine and... 2006The BK Virus (BKV) genome is a double-stranded, circular DNA molecule with genetic organization similar to other polyomaviruses, and high homology to JC Virus (JCV) and... (Review)
Review
The BK Virus (BKV) genome is a double-stranded, circular DNA molecule with genetic organization similar to other polyomaviruses, and high homology to JC Virus (JCV) and SV40. The archetypal form of BKV noncoding regulatory region (NCRR) is the infectious form of BKV that replicates in the urothelium and is excreted in the urine. Rearranged forms of the NCRR are found in kidney and other tissues often in association with disease. BKV strains can be assigned to genotype/serotype groups based on sequence variation in the VP1 gene. Sequencing of the complete genomes from patient samples will enhance BKV phylogenetic studies and identify genotypic differences and naturally occurring mutations in BKV that may correlate with incidence and/or severity of a disease. This chapter is a review of the molecular genetics of the BK virus in respect to BKV disease.
Topics: BK Virus; Molecular Biology; Papillomavirus Infections
PubMed: 16626029
DOI: 10.1007/0-387-32957-9_6 -
Reviews in Medical Virology Jul 2020BK polyomavirus (BKPyV or BKV) is a non-enveloped, circular double-stranded DNA virus that may exceed 80% seroprevalence in adults. BKV infection typically occurs during... (Review)
Review
BK polyomavirus (BKPyV or BKV) is a non-enveloped, circular double-stranded DNA virus that may exceed 80% seroprevalence in adults. BKV infection typically occurs during childhood, and the majority of adults are latently infected. While BKV infection is rarely associated with clinical disease in most individuals, in immunosuppressed individuals, reactivation may cause kidney (BK-associated nephropathy) or bladder (hemorrhagic cystitis and ureteral stenosis) injury. No antiviral therapies have been approved for the treatment of BKV infection. Reducing immunosuppression is the most effective therapy, although this is not feasible in many patients. Thus, a robust understanding of viral pathogenesis and viral diversity remains important for the development of future therapeutic strategies. Studies of BKV diversity are quite sparse compared to other common viral infections; thus, much of our understanding of BVK variability and evolution relies heavily analogous studies of other viruses such as HIV or viral hepatitis. We provide a comprehensive review of BKV diversity at the population and individual level with careful consideration of how viral variability may impact viral replication, pathogenesis, tropism, and protein function. We also discuss a number of outstanding questions related to BK virus diversity that should be explored rigorously in future studies.
Topics: Animals; BK Virus; Biodiversity; Evolution, Molecular; Genetic Variation; Genome, Viral; Genomics; Humans; Phylogeny; Polyomavirus Infections
PubMed: 32128960
DOI: 10.1002/rmv.2102 -
Indian Journal of Medical Microbiology 2018BK virus (BKV) is an opportunistic pathogen which causes significant morbidity and mortality in individuals who are immunodeficient. We aimed to quantitate and...
PURPOSE
BK virus (BKV) is an opportunistic pathogen which causes significant morbidity and mortality in individuals who are immunodeficient. We aimed to quantitate and characterise BKV and to correlate with the degree of immunosuppression among human immunodeficiency virus (HIV)-1-infected individuals.
METHODS
BKV DNA detection was carried out using an in-house quantitative real-time polymerase chain reaction on paired whole-blood and urine samples collected from 187 antiretroviral therapy (ART)-naïve HIV-1-infected individuals and 93 healthy individuals who served as controls. Sequencing was performed for a proportion of high BK viral load (VL) samples to observe non-coding control region (NCCR) rearrangements.
RESULTS
BKV positivity in urine was 25.6% among HIV-infected individuals and 10.7% in control individuals (P = 0.03). The BK VL showed a significant negative correlation with CD4+ T-cell counts, a positive correlation with WHO clinical staging and no significant correlation with HIV-1 VL. Of 42 BKVs from urine samples sequenced, two showed rearrangements without clinically severe disease or high VL. Their NCCR and VP1 sequence-based genotyping revealed genotype I. In a small subset of individuals (n = 8) on ART who were being followed up, six individuals showed either decrease or complete clearance of virus with ART.
CONCLUSION
There was a higher frequency of BK viruria in HIV-1-infected individuals than among healthy controls and the positivity correlated with the degree of immunosuppression. There was no association of high VL with NCCR rearrangements in urine.
Topics: Adult; BK Virus; CD4 Lymphocyte Count; CD4-Positive T-Lymphocytes; Female; HIV Infections; HIV-1; Humans; Immunosuppression Therapy; Male; Polyomavirus Infections; Viral Load
PubMed: 30084406
DOI: 10.4103/ijmm.IJMM_18_54 -
Transplant Infectious Disease : An... Jun 2006BK virus (BKV) is a small, non-enveloped, double-stranded DNA virus and a member of the Polyomaviridae family. As the recently recognized etiologic agent of... (Review)
Review
BK virus (BKV) is a small, non-enveloped, double-stranded DNA virus and a member of the Polyomaviridae family. As the recently recognized etiologic agent of polyomavirus-associated nephropathy, the events involved in BKV invasion of host cells are an important area of study. Using cell culture models, the mechanism by which BKV infects permissive hosts to gain access to the replication machinery within these cells is beginning to unfold. BKV uses an N-linked glycoprotein containing an alpha(2,3)-linked sialic acid as a receptor. After this initial attachment, BKV enters cells through caveolae-mediated endocytosis. Intracellular trafficking via cellular cytoskeletal components follows this relatively slow and cholesterol-dependent internalization. BKV must reach the nucleus for viral transcription and replication to occur. Elucidating the steps of the early viral lifecycle would provide clues to help explain the infectious spread and pathology of this human pathogen.
Topics: Animals; BK Virus; Endocytosis; Humans; Polyomavirus Infections; Receptors, Virus
PubMed: 16734628
DOI: 10.1111/j.1399-3062.2006.00153.x -
Ultrastructural Pathology 2005BK polyomavirus has become an important etiologic agent responsible for significant morbidity in renal transplant recipients. This virus can be detected in transitional... (Review)
Review
BK polyomavirus has become an important etiologic agent responsible for significant morbidity in renal transplant recipients. This virus can be detected in transitional cells in the urine (decoy cells) using cytology, but correlation with allograft function status and histologic evidence of renal involvement is poor. Accurate diagnosis of BK polyomavirus infection requires a high index of suspicion and utilization of ancillary diagnostic techniques in many cases. Electron microscopy is very sensitive in depicting the presence of BK virions, but the finding of viral particles is not by itself diagnostic of BK interstitial nephritis. Management of patients with polyoma virus nephropathy is difficult since there is no specific antiviral therapy available at this time.
Topics: Animals; BK Virus; Humans; Immunohistochemistry; In Situ Hybridization; Kidney; Kidney Transplantation; Microscopy, Electron, Transmission; Polymerase Chain Reaction; Polyomavirus Infections; Tumor Virus Infections; Virion
PubMed: 16316947
DOI: 10.1080/01913120500323399 -
BMC Infectious Diseases Aug 2020BK virus-associated nephropathy (BKVAN) is a relatively common cause of renal dysfunction in the first six months after renal transplantation. It arises from...
BACKGROUND
BK virus-associated nephropathy (BKVAN) is a relatively common cause of renal dysfunction in the first six months after renal transplantation. It arises from reactivation of the latent and usually harmless BK virus (BK virus) due to immunosuppression and other factors including some that are unique to renal transplantation such as allograft injury. BKVAN is much rarer in non-renal solid organ transplantation, where data regarding diagnosis and management are extremely limited.
CASE PRESENTATION
We report a case of a 58-year-old man found to have worsening renal dysfunction nine months after bilateral sequential lung transplantation for chronic obstructive pulmonary disease (COPD). He had required methylprednisolone for acute allograft rejection but achieved good graft function. Urine microscopy and culture and renal ultrasound were normal. BK virus PCR was positive at high levels in urine and blood. Renal biopsy subsequently confirmed BKVAN. The patient progressed to end-stage renal failure requiring haemodialysis despite reduction in immunosuppression, including switching mycophenolate for everolimus, and the administration of intravenous immunoglobulin (IVIG).
CONCLUSIONS
This very rare case highlights the challenges presented by BK virus in the non-renal solid organ transplant population. Diagnosis can be difficult, especially given the heterogeneity with which BKV disease has been reported to present in such patients, and the optimal approach to management is unknown. Balancing reduction in immunosuppression against prevention of allograft rejection is delicate. Improved therapeutic options are clearly required.
Topics: BK Virus; DNA, Viral; Humans; Immunoglobulins, Intravenous; Immunosuppressive Agents; Kidney Transplantation; Lung Transplantation; Male; Methylprednisolone; Middle Aged; Mycophenolic Acid; Polyomavirus Infections; Pulmonary Disease, Chronic Obstructive; Tumor Virus Infections
PubMed: 32795251
DOI: 10.1186/s12879-020-05292-0