Cytomegalovirus and polyomavirus BK posttransplant

Egli, Adrian; Binggeli, S.; Bodaghi, Sohrab; Dumoulin, Alexis; Funk, Georg A.; Khanna, Nina; Leuenberger, David; Gosert, Rainer; Hirsch, Hans H.

doi:10.1093/ndt/gfm868

Cited by 39 publications

(47 citation statements)

References 73 publications

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“…5 It is caused by the reactivation of BKV infection in the allograft, which excites an interstitial nephritis, 6 and presents with clinically asymptomatic, slowly progressive allograft failure in 50-90% of cases. 4 The urinalysis is consistent with an interstitial nephritis with the passage of decoy cells, and definitive diagnosis requires tissue biopsy. 2,7 In severe cases, progressive irreversible damage amounts to subsequent graft loss.…”

Section: Introductionmentioning

confidence: 98%

“…3 Asymptomatic intermittent viral replication with active shedding occurs in some immunocompetent individuals. 4 PVAN occurs in up to 10% of renal transplantation, 2,4 most commonly within the first 2 years. 5 It is caused by the reactivation of BKV infection in the allograft, which excites an interstitial nephritis, 6 and presents with clinically asymptomatic, slowly progressive allograft failure in 50-90% of cases.…”

Section: Introductionmentioning

confidence: 99%

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Quantification of BK Viral Load in Asymptomatic Renal Allograft Recipients

Chan¹,

Leung²,

Wong³

et al. 2012

Renal Failure

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Introduction: Polyoma BK virus (BKV) has recently been identified to cause renal allograft dysfunction, which manifests as polyomavirus-associated nephropathy (PVAN). However, the presence and level of BKV DNA in renal allograft patients with good and stable renal function have remained undetermined. Methods: In this prospective study, serum samples were collected from a total of 45 renal allograft recipients with serum creatinine <155 μmol/L. In 17 patients, whose duration of transplantation was under 2 years, samples were collected at 3-4-month intervals for up to 2 years after transplantation. BK viral load was quantified using quantitative polymerase chain reaction (Q-PCR). Results: The BK viral load in asymptomatic renal allograft recipients was independent of the duration of transplantation and did not correlate with allograft function. The mean (AE SD) level of viremia was 552.80 AE 1931.00 genome copies/mL, with 92.9% of patients having low levels of viremia corresponding to <1 Â 10 3 copies/mL. In contrast, patients with proven PVAN had levels in the range of 10 6 copies/mL. Conclusions: The prevailing BK viral load in asymptomatic renal allograft patients is quantifiably low. Our findings may guide optimal immunosuppressive modulation in PVAN cases, where judicious manipulation of immunosuppression is required without inciting allograft rejection.

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Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Quantification of BK Viral Load in Asymptomatic Renal Allograft Recipients

Chan¹,

Leung²,

Wong³

et al. 2012

Renal Failure

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“…The median frequency of CMV-specific CD8+ cells was significantly higher in a group of 27 heart and lung transplant patients in cases that did not developed CMV-disease [11] . Moreover, in a study on 73 renal transplant recipients, also the median frequency of CMV-specific CD4+ cells was significantly higher in patients that did not developed CMV disease [12,13] . Gerna and coll.…”

Section: Role Of Virus-specific Cellular Immune Response In Transplanmentioning

confidence: 92%

Evaluation of virus-specific cellular immune response in transplant patients

Costa

Saldan²,

Cavallo³

2012

WJV

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Virus-specific immune responses have a major impact on the outcome of the infection. Viral agents that are characterized by latency, such as herpesviruses and polyomaviruses, require a continuous immune control to reduce the extent of viral reactivation, as viral clearance cannot be accomplished, independently from the anti-viral treatment. In transplant patients, morbidity and mortality related to viral infections are significantly increased. In fact, the key steps of activation of T-cells are major target for anti-rejection immunosuppressive therapy and anti-viral immune response may be altered when infected cells and cellular effectors of immune response coexist in a transplanted organ. The role of cellular immune response in controlling viral replication and the main methods employed for its evaluation will be discussed. In particular, the main features, including both advantages and limitations, of available assays, including intracellular cytokine staining, major histocompatibility complex -multimer-based assays, Elispot assay, and QuantiFERON test, will be described. The potential applications of these assays in the transplant context will be discussed, particularly in relation to cytomegalovirus and polyomavirus BK infection. The relevance of introducing viro-immunological monitoring, beside virological monitoring, in order to identify the risk profile for viral infections in the transplant patients will allows for define a patient-tailored clinical management, particular in terms of modulation of immunosuppressive therapy and anti-viral administration.

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“…In the absence of malignancy, this would suggest a viral infection of the uroepithelium. Pathogens include cytomegalovirus, BK, or adenovirus, all known causes of hemorrhagic cystitis (16,17).…”

Section: Clinical Differentialmentioning

confidence: 99%