Viral Impact on Long-term Kidney Graft Function

Helanterä, Ilkka; Egli, Adrian; Koskinen, Petri; Lautenschlager, Irmeli; Hirsch, Hans H.

doi:10.1016/j.idc.2010.02.003

Cited by 41 publications

(39 citation statements)

References 257 publications

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“…The careful use of this distinct terminology is consistent with the current clinical practice for other viruses, e.g., HIV-1 infection, replication, and disease, and applies also to other viruses such as Hepatitis B or cytomegalovirus (CMV) (67)(68)(69) (6,28,(76)(77)(78)(79). By contrast, the seroreactivity to the closely related BKPyV reaches more than 95% during early childhood, followed by slow decline in titers toward the fifth decade of life (6,28,(76)(77)(78)(79)(80).…”

Section: Clinical Implications Definition Of Infection Replication mentioning

confidence: 56%

The human JC polyomavirus (JCPyV): virological background and clinical implications

Hirsch

Kardas

Kranz

et al. 2013

APMIS

Self Cite

149

169

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JC polyomavirus (JCPyV) was the first of now 12 PyVs detected in humans, when in 1964, PyV particles were revealed by electron microscopy in progressive multifocal leukoencephalopathy (PML) tissues. JCPyV infection is common in 35–70% of the general population, and the virus thereafter persists in the renourinary tract. One third of healthy adults asymptomatically shed JCPyV at approximately 50 000 copies/mL urine. PML is rare having an incidence of <0.3 per 100 000 person years in the general population. This increased to 2.4 per 1000 person years in HIV‐AIDS patients without combination antiretroviral therapy (cART). Recently, PML emerged in multiple sclerosis patients treated with natalizumab to 2.13 cases per 1000 patients. Natalizumab blocks α4‐integrin‐dependent lymphocyte homing to the brain suggesting that not the overall cellular immunodeficiency but local failure of brain immune surveillance is a pivotal factor for PML. Recovering JCPyV‐specific immune control, e.g., by starting cART or discontinuing natalizumab, significantly improves PML survival, but is challenged by the immune reconstitution inflammatory syndrome. Important steps of PML pathogenesis are undefined, and antiviral therapies are lacking. New clues might come from molecular and functional profiling of JCPyV and PML pathology and comparison with other replicative pathologies such as granule cell neuronopathy and (meningo‐)encephalitis, and non‐replicative JCPyV pathology possibly contributing to some malignancies. Given the increasing number of immunologically vulnerable patients, a critical reappraisal of JCPyV infection, replication and disease seems warranted.

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Section: Clinical Implications Definition Of Infection Replication mentioning

confidence: 56%

The human JC polyomavirus (JCPyV): virological background and clinical implications

Hirsch

Kardas

Kranz

et al. 2013

APMIS

Self Cite

149

169

View full text Add to dashboard Cite

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“…Together this indicates a markedly increased overall viral burden, which might induce more allograft damage due to direct and indirect effects (39). Although allograft function remained stable in patients with definitive PyVAN, these favorable results need to be confirmed in a larger population with longer follow-up.…”

Section: Schaub Et Almentioning

confidence: 95%

Reducing Immunosuppression Preserves Allograft Function in Presumptive and Definitive Polyomavirus-Associated Nephropathy

Schaub

Hirsch

Dickenmann

et al. 2010

American Journal of Transplantation

228

217

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Early detection of polyomavirus BK (BKV) viremia and reduction of immunosuppression is recommended forBased on subsequent allograft biopsy results and peak BKV-viremia, patients were assigned to three groups: (i) definitive PyVAN (n = 13), (ii) presumptive PyVAN defined by plasma BKV-loads of ≥4 log 10 copies/ml (n = 17) and (iii) low BKV-viremia (n = 8). Clearance of BKV-viremia was achieved in 35/38 patients (92%) and subsequent clinical rejection occurred in 3/35 patients (8.6%), both without any difference among the groups. Patients with definitive Py-VAN had higher peak plasma BKV-loads and required longer time for clearance (8.8 vs. 4.6 vs. 2.9 months; p = 0.001). However, allograft function remained stable from baseline to last follow-up at 34 months (range 18-60) in all three groups with median serum creatinine of 1.6 mg/dl, 1.6 mg/dl and 1.3 mg/dl, respectively. We conclude that screening for BKV-replication and reduction of immunosuppression is an effective strategy to preserve medium-term allograft function even in patients developing definitive PyVAN.

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“…BKV replication appears to induce the production of proinflammatory and profibrotic cytokines (e.g. TGF-b) that participate in the development of chronic allograft fibrosis observed in the later stages of BKVassociated nephropathy (25).…”

Section: Type Of Organ Transplantmentioning

confidence: 99%

The Impact of Infection on Chronic Allograft Dysfunction and Allograft Survival After Solid Organ Transplantation

Martín-Gandul

Mueller

Pascual

et al. 2015

American Journal of Transplantation

134

103

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Infectious diseases after solid organ transplantation (SOT) are a significant cause of morbidity and reduced allograft and patient survival; however, the influence of infection on the development of chronic allograft dysfunction has not been completely delineated. Some viral infections appear to affect allograft function by both inducing direct tissue damage and immunologically related injury, including acute rejection. In particular, this has been observed for cytomegalovirus (CMV) infection in all SOT recipients and for BK virus infection in kidney transplant recipients, for community-acquired respiratory viruses in lung transplant recipients, and for hepatitis C virus in liver transplant recipients. The impact of bacterial and fungal infections is less clear, but bacterial urinary tract infections and respiratory tract colonization by Pseudomonas aeruginosa and Aspergillus spp appear to be correlated with higher rates of chronic allograft dysfunction in kidney and lung transplant recipients, respectively. Evidence supports the beneficial effects of the use of antiviral prophylaxis for CMV in improving allograft function and survival in SOT recipients. Nevertheless, there is still a need for prospective interventional trials assessing the potential effects of preventive and therapeutic strategies against bacterial and fungal infection for reducing or delaying the development of chronic allograft dysfunction.

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Viral Impact on Long-term Kidney Graft Function

Cited by 41 publications

References 257 publications

The human JC polyomavirus (JCPyV): virological background and clinical implications

The human JC polyomavirus (JCPyV): virological background and clinical implications

Reducing Immunosuppression Preserves Allograft Function in Presumptive and Definitive Polyomavirus-Associated Nephropathy

The Impact of Infection on Chronic Allograft Dysfunction and Allograft Survival After Solid Organ Transplantation

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