Reactivation of BK Virus in the Early Period After Kidney Transplantation

Ziedina, Ieva; Folkmane, Inese; Chapenko, Svetlana; Murovska, Modra; Sultanova, Alina; Jushinskis, Janis; Rozental, Rafail

doi:10.1016/j.transproceed.2009.01.036

Cited by 13 publications

(13 citation statements)

References 7 publications

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“…The potential risk factors for polyoma virus are numerous. Retransplantation, body mass index >30 kg/m 2 , and tacrolimus use are all noted risk factors for polyoma viremia (15). Additionally, recurrent episodes of rejection and high‐dose immunosuppressant therapy predispose to PVN (29, 30).…”

Section: Discussionmentioning

confidence: 99%

“…Unfortunately, the prognosis is poor once true PVN develops (14). PVN can be seen as early as 3 months after transplantation (15) with up to one-third of patients experiencing irreversible graft failure within 1 year of diagnosis. Moreover, allografts that survive 41 year from diagnosis of PVN often experience signi¢cant deterioration in function and decreased long-term survival (3,7,10,16,17 ).…”

mentioning

confidence: 99%

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Initiation of a screening protocol for polyoma virus results in a decreased rate of opportunistic non‐BK viral disease after renal transplantation

Koleilat

Kushnir

Gallichio

et al. 2010

Transplant Infectious Dis

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Initiation of a screening protocol for polyoma virus results in a decreased rate of opportunistic non‐BK viral disease after renal transplantation

Koleilat

Kushnir

Gallichio

et al. 2010

Transplant Infectious Dis

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“…JCPyV replication and viral protein expression are higher in immunosuppressed patients and are inversely related to CD4 + cell count . Additionally, the increased use of potent immunosuppressive agents, for example tacrolimus, has been identified as a promoting factor for BKPyV reactivation after kidney transplantation . While 42% of patients with TS were exposed to tacrolimus, whether tacrolimus treatment influences TSPyV reactivation is not clear.…”

Section: Association With Immunosuppression Is Characteristic Of Polymentioning

confidence: 99%

Molecular insight into the viral biology and clinical features of trichodysplasia spinulosa

Nguyen

Rády

et al. 2016

British Journal of Dermatology

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Trichodysplasia spinulosa (TS) is a disfiguring skin disease that occurs most frequently in patients receiving immunosuppressive therapies, and is thus frequently associated with organ transplantation. TS is characterized clinically by folliculocentric papular eruption, keratin spine formation and development of leonine face; and histologically by expansion of the inner root sheath epithelium and high expression of the proliferative marker Ki-67. Recent discovery of the TS-associated polyomavirus (TSPyV) and emerging studies demonstrating the role of TSPyV tumour antigens in cell proliferation pathways have opened a new corridor for research on TS. In this brief review, we summarize the clinical and histological features of TS and evaluate the current options for therapy. Furthermore, we address the viral aetiology of the disease and explore the mechanisms by which TSPyV may influence TS development and progression. As reports of TS continue to rise, clinician recognition of TS, as well as accompanying research on its underlying pathogenesis and therapeutic options, is becoming increasingly important. It is our hope that heightened clinical suspicion for TS will increase rates of diagnosis and will galvanize both molecular and clinical interest in this disease.

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“…Following renal transplantation, reactivation of BKV demonstrated by BK viruria is usually noticed after 3-6 mo while reactivation of JCV occurs as early as five days post transplantation[ 379 ]. Early BKV reactivation is associated with viremia[ 377 ] and worse transplant function[ 372 ].…”

Section: Pathogenesis Of Bkv Infection[ 10 mentioning

confidence: 99%

“…After entry into the cytoplasm, BKV is transported into the endoplasmic reticulum along the microtubules by a complex mechanism favored by acidic environment[ 368 ]. The ER associated degradation (ERAD) pathway, which is responsible for the transfer to the cytosol of ER secretory proteins that have not attained their proper conformation, where they are degraded by proteasomes, is responsible for transfering BKV into the cytosol, followed by entry of these proteins into the nucleus[ 372 ]. After entry of BKV into the nucleus, BKV genome release takes place[ 383 ].…”

Section: Pathogenesis Of Bkv Infection[ 10 mentioning

confidence: 99%

BK nephropathy in the native kidneys of patients with organ transplants: Clinical spectrum of BK infection

Vigil

Konstantinov

Barry

et al. 2016

WJT

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Nephropathy secondary to BK virus, a member of the Papoviridae family of viruses, has been recognized for some time as an important cause of allograft dysfunction in renal transplant recipients. In recent times, BK nephropathy (BKN) of the native kidneys has being increasingly recognized as a cause of chronic kidney disease in patients with solid organ transplants, bone marrow transplants and in patients with other clinical entities associated with immunosuppression. In such patients renal dysfunction is often attributed to other factors including nephrotoxicity of medications used to prevent rejection of the transplanted organs. Renal biopsy is required for the diagnosis of BKN. Quantitation of the BK viral load in blood and urine are surrogate diagnostic methods. The treatment of BKN is based on reduction of the immunosuppressive medications. Several compounds have shown antiviral activity, but have not consistently shown to have beneficial effects in BKN. In addition to BKN, BK viral infection can cause severe urinary bladder cystitis, ureteritis and urinary tract obstruction as well as manifestations in other organ systems including the central nervous system, the respiratory system, the gastrointestinal system and the hematopoietic system. BK viral infection has also been implicated in tumorigenesis. The spectrum of clinical manifestations from BK infection and infection from other members of the Papoviridae family is widening. Prevention and treatment of BK infection and infections from other Papovaviruses are subjects of intense research.

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Reactivation of BK Virus in the Early Period After Kidney Transplantation

Cited by 13 publications

References 7 publications

Initiation of a screening protocol for polyoma virus results in a decreased rate of opportunistic non‐BK viral disease after renal transplantation

Initiation of a screening protocol for polyoma virus results in a decreased rate of opportunistic non‐BK viral disease after renal transplantation

Molecular insight into the viral biology and clinical features of trichodysplasia spinulosa

BK nephropathy in the native kidneys of patients with organ transplants: Clinical spectrum of BK infection

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