Pretransplantation seroreactivity in kidney donors and recipients as a predictive factor for posttransplant BKPyV-DNAemia

Saláková, Martina; Ludvı́ková, Viera; Hamšíková, Eva; Kolářová, Marie; Šroller, Vojtěch; Viklický, Ondřej; Wohlfahrtová, Mariana

doi:10.3389/fimmu.2022.929946

Cited by 3 publications

(2 citation statements)

References 26 publications

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“…These findings are consistent with the those of Saláková et al. ( 16 ) who established a significant correlation between donor seropositivity and recipient post-transplant BKV infection. A trend toward donor seropositivity and BKVAN was observed in their study, but lacked statistical significance.…”

Section: Discussionsupporting

confidence: 93%

“…Recently, Saláková et al. reported that the donor BKV-IgG seroprevalence and antibody level were strongly associated with posttransplant BK viremia and BKVAN in a study of 210 KTRs and 130 donors ( 16 ). Finally, they confirmed recommendation by Hirsh and Randhawa that KTRs from seropositive donors should be routinely screened for BKV-DNA in plasma much more frequently than KTRs from seronegative donors ( 5 ).…”

Section: Introductionmentioning

confidence: 99%

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Pretransplant BKV-IgG serostatus and BKV-specific ELISPOT assays to predict BKV infection after kidney transplantation

Bae,

Jung,

Chung

et al. 2023

Front. Immunol.

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IntroductionPolyomavirus (BKV) infection can lead to major complications and damage to the graft in kidney transplant recipients (KTRs). We investigated whether pretransplant BK serostatus and BK-specific cell-mediated immunity (CMI) predicts post-transplant BK infection.MethodsA total of 93 donor-recipient pairs who underwent kidney transplantation (KT) and 44 healthy controls were examined. Assessment of donor and recipient BKV serostatus and BKV-CMI in recipients was performed prior to transplantation using BKV-IgG ELISA and BKV-specific IFN-g ELISPOT assays against five BK viral antigens (LT, St, VP1, VP2, and VP3). BK viremia was diagnosed when blood BKV-DNA of 104 copies/mL or more was detected during follow-up periods. ResultsAnti-BKV IgG antibody was detected in 74 (79.6%) of 93 KTRs and in 68 (73.1%) of 93 KT donors. A greater percentage of KTRs who received allograft from donors with high levels of anti-BKV IgG had posttransplant BK viremia (+) than KTRs from donors with low anti-BKV IgG (25.5% [12/47] vs. 4.3% [2/46], respectively; P = 0.007). Pretransplant total BKV-ELISPOT results were lower in BK viremia (+) patients than in patients without viremia (-) 20.5 [range 9.9−63.6] vs. 72.0 [43.2 - 110.8]; P = 0. 027). The sensitivity and specificity of the total BKV-ELISPOT assay (cut-off ≤ 53 spots/3×105 cells) for prediction of posttransplant BK viremia were 71.4 (95% CI: 41.9–91.6) and 54.4 (42.8–65.7), respectively. The combination of high donor BKV-IgG, low recipient BKV-IgG, and low total BKV-ELISPOT results improved specificity to 91.1%.DiscussionOur study highlights the importance of pretransplant BKV-IgG serostatus and BKV-specific CMI in predicting posttransplant BKV infection in KTRs. The combination of high donor BKV-IgG, low recipient BKV-IgG, and low total BKV-ELISPOT results predicted BK viremia after KT. Pretransplant identification of patients at highrisk for BK viremia could enable timely interventions and improve clinical outcomes of KTRs.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Pretransplant BKV-IgG serostatus and BKV-specific ELISPOT assays to predict BKV infection after kidney transplantation

Bae,

Jung,

Chung

et al. 2023

Front. Immunol.

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Neutralizing Antibodies Targeting BK Polyomavirus

Helle,

Aubry,

Morel

et al. 2024

JASN

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The majority of the world’s adult population is latently infected by the BK polyomavirus. It causes asymptomatic infection in healthy individuals but emerged as a threat to kidney transplant recipients because of virus associated nephropathy caused by immunosuppressive therapy. In these conditions, when a functional cellular response is impaired by immunosuppression, neutralizing antibodies may play a major role, since they can directly prevent infection of target cells, independently of cell mediated immunity, by binding to the viral particles. Studying the contribution of anti-BK virus neutralizing antibodies in viral control has long been hampered by the lack of convenient in vitro models but major progress has been made in the last decade. The four BK virus genotypes have been demonstrated to behave as distinct serotypes. A low recipient neutralizing antibody titer against the donor’s serotype before kidney transplant has been significantly associated with BK virus replication after transplant. Different mechanisms exploited by the BK virus to evade neutralizing antibodies have been described. Recent studies also support the potential benefit of administering intravenous immunoglobulins or monoclonal neutralizing antibodies as a therapeutic strategy and, more interestingly, this could also be used as preventive or pre-emptive therapy, before advanced kidney damage has occurred. Besides, neutralizing antibodies could be induced by vaccination. In this review, we summarize accumulated knowledge on anti-BK virus neutralizing antibodies as well as their clinical importance and therapeutic potential for kidney transplant recipients.

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BK Virus-Associated Nephropathy in Adult Patients Post Kidney Transplantation: What Progress in 30 Years of History?

Bentata

2024

OBM Transplant

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Completely unknown before the 90s and exceptional up to the 2000s, BK virus nephropathy (BKvN), usually known as polyomavirus-associated nephropathy, has emerged as a significant and severe viral complication in kidney transplantation (KT). More than twenty years after Gardner's discovery of BKv in 1971, Purighalla described, in 1995, the first case of BKvN. Four years later in 1999, Nickeleit et al. published a first series of five cases of BKvN and made very precious and pertinent contributions to understanding this new entity. It has been well established that in post-KT, 30 to 50% of kidney transplant recipients are positive for BK viruria, of whom approximately one-third will develop BK viremia and, without intervention, could progress in 1 to 10% of cases to BKvN, leading to kidney graft failure in more than half of the cases. For now, there is no preventive antiviral treatment for BKvN; only a strategy of rapid, efficient screening allows for the preservation of renal graft function. The only effective and sure treatment measure is to reduce the intensity of total immunosuppression, including immunosuppressive drugs and corticosteroids. Based on the current data, this review describes the physiopathology, diagnosis, and management of BKvN in adult KTRs. It presents the results of the fifty most important studies published during the last two decades.

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Pretransplantation seroreactivity in kidney donors and recipients as a predictive factor for posttransplant BKPyV-DNAemia

Cited by 3 publications

References 26 publications

Pretransplant BKV-IgG serostatus and BKV-specific ELISPOT assays to predict BKV infection after kidney transplantation

Pretransplant BKV-IgG serostatus and BKV-specific ELISPOT assays to predict BKV infection after kidney transplantation

Neutralizing Antibodies Targeting BK Polyomavirus

BK Virus-Associated Nephropathy in Adult Patients Post Kidney Transplantation: What Progress in 30 Years of History?

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