A Prospective Longitudinal Study of BK Virus Infection in 104 Renal Transplant Recipients

Bressollette-Bodin, Céline; Coste‐Burel, Marianne; Hourmant, Maryvonne; Sebille, Véronique; André-Garnier, Élisabeth; Imbert-Marcille, Berthe-Marie

doi:10.1111/j.1600-6143.2005.00934.x

Cited by 188 publications

(146 citation statements)

References 41 publications

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“…Patients with biopsy-proven BKVAN showed a higher median viral load than patients without BKVAN. Corresponding to the predictive value of 2.5Eþ07 copies/ml, we found a median viral load of 3.20Eþ08 copies/ml in patients with BKVAN [Hirsch et al, 2002;Bressollette-Bodin et al, 2005]. However, the high titer is independent of the subtype or mutations in the VP1 loops.…”

Section: Discussionsupporting

confidence: 54%

“…High titers in urine and plasma can be considered as predictive markers for BKV-associated nephropathy. The proposed threshold for viruria as a predictive value for BKVAN is >2.5Eþ07 BKV copies/ ml, and the viremic threshold is >1.6Eþ04 BKV copies/ ml [Drachenberg et al, 2004[Drachenberg et al, , 2007Bressollette-Bodin et al, 2005;Funk et al, 2006;Viscount et al, 2007;Costa et al, 2008]. The reasons for the reactivation of BKV are not well understood.…”

Section: Introductionmentioning

confidence: 99%

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Mutations in the BC‐loop of the BKV VP1 region do not influence viral load in renal transplant patients

Krautkrämer

Klein

Sommerer

et al. 2008

Journal of Medical Virology

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The reactivation and replication of the BK polyomavirus (BKV) leading to BKV-associated nephropathy (BKVAN) is one of the major complications in renal transplantation patients. BKV isolates were classified into four subtypes (I-IV) based on genotype variations within the VP1-coding region. The type-specific amino acid differences cluster within the BC-loop of the major capsid protein VP1. As demonstrated in vitro, mutations in this region also play a role in the infectivity, attachment and stability of viral particles. Therefore, we analyzed the prevalence of BC-loop mutations in isolates of kidney transplant patients and compared their viral load in the urine. The VP1 subtyping regions of BKV isolates obtained from urine samples of 45 renal transplant patients were sequenced. The phylogenetic analysis of these sequences revealed that subtype I (66.67%) is the most prevalent genotype. The remaining isolates belong to subtype IV (33.33%). A high frequency of changes to specific amino acids within the BC-loop was identified among the BKV isolates from renal transplant patients. Patients with BKVAN exhibited a higher viral replication than patients without nephropathy. Although titers of isolates of subtype I were higher than titers of subtype IV isolates, the difference did not reach statistical significance. In addition, amino acid changes in the BC-loop did not influence the viral load and the incidence of BKVAN. These in vivo results demonstrate that high replication rates which serve as a predictive marker for BKVAN are not caused by altered receptor binding or affinity via mutated BC-loops.

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Section: Discussionsupporting

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Mutations in the BC‐loop of the BKV VP1 region do not influence viral load in renal transplant patients

Krautkrämer

Klein

Sommerer

et al. 2008

Journal of Medical Virology

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“…Reactivation of BK virus is a frequent phenomenon after kidney transplantation, with BK virus copies identified in blood and urine of 30–50% of patients during the first year after transplantation 35. BK virus encodes a single precursor microRNA, bkv‐miR‐B1, which generates a mature ‐3p and ‐5p variant 36.…”

Section: Virally Encoded Micrornas In Kidney Transplantationmentioning

confidence: 99%

Urinary MicroRNA as Biomarker in Renal Transplantation

Vrie

Deegens

Eikmans

et al. 2017

American Journal of Transplantation

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Urine represents a noninvasive source in which proteins and nucleic acids can be assessed. Such analytes may function as biomarkers to monitor kidney graft pathology at every desired frequency, thereby providing a time window to prevent graft damage by therapeutic intervention. Recently, several proteins have been measured in urine as markers of graft injury. However, the specificity is limited, and measuring urinary proteins generally lacks the potential to predict early kidney graft damage. Currently, urinary mRNA and microRNA are being investigated to evaluate the prognostic value of changes in gene expression during the initial stages of graft damage. At such time point, a change in treatment regimen and dosage is expected to have maximum potency to minimize future decline in graft function. Both mRNA and microRNAs have shown promising results in both detection and prediction of graft injury. An advantage of microRNAs compared to mRNA molecules is their stability, a characteristic that is beneficial when working with urine samples. In this review, we provide the current state of urinary biomarkers in renal transplantation, with a focus on urinary microRNA. In addition, we discuss the methods used to study urinary microRNA expression.

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“…Persistence of BK virus shedding (decoy cells or DNA loads Ͼ10 7 /ml) rather than isolated/episodic detection has been shown to identify patients who are at risk for BKPVAN (18,27). Although viral replication in the renourinary tract (expressed as viruria) is observed in 30 to 40% of patients in the first 6 mo posttransplantation, significant viremia develops in significantly fewer patients (12 to 15%), and further progression to BKPVAN is even more rare (Յ10%) (30,(32)(33)(34)(35).…”

Section: Screening For Prevention Of Bkpvanmentioning

confidence: 99%

Histologic versus Molecular Diagnosis of BK Polyomavirus–Associated Nephropathy

Drachenberg

Papadimitriou²,

Ramos³

2006

Clinical Journal of the American Society of Nephrology

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Although discovered in 1970 the BK virus infections had no significant clinical impact until the emergence of BK virusassociated allograft nephropathy (BKPVAN). Escalating clinical challenges required better diagnostic tools and delineation of uniform criteria for diagnosis. In recent years, the widespread use of real-time PCR for measuring viral loads has confirmed that BK viruria and viremia are consistently identified before the development of overt nephritis. The identification of this viruria-viremia-nephritis sequence has provided tools for screening renal transplant patients and the possibility of earlier intervention with improved outcomes. Analysis of current clinical trends indicates that despite the fact that a positive renal biopsy is the "gold standard" for the diagnosis of BKPVAN, clinical interventions often are based on the surrogate markers of the disease rather than on tissue diagnosis. This is conceptually supported by the fact that early BKPVAN is focal and liable to tissue sampling errors. Strong arguments remain, however, in favor of retaining the requirement for tissue evaluation in patients who are suspected of having BKPVAN. BKPVAN selectively affects the graft and is likely to occur in a background of immune and/or nonimmune renal injury. A renal biopsy is necessary to exclude other pathologic processes (e.g., acute rejection) that could coexist with BKPVAN or be the main cause of allograft dysfunction. Evaluation of a renal biopsy for the purpose of staging is important for prognosis and is also of paramount importance for the rational assessment of therapeutic success.

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A Prospective Longitudinal Study of BK Virus Infection in 104 Renal Transplant Recipients

Cited by 188 publications

References 41 publications

Mutations in the BC‐loop of the BKV VP1 region do not influence viral load in renal transplant patients

Mutations in the BC‐loop of the BKV VP1 region do not influence viral load in renal transplant patients

Urinary MicroRNA as Biomarker in Renal Transplantation

Histologic versus Molecular Diagnosis of BK Polyomavirus–Associated Nephropathy

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