Clinical Course of Polyoma Virus Nephropathy in 67 Renal Transplant Patients

Ramos, Emilio; Drachenberg, Cinthia B.; Papadimitriou, John C.; Hamze, Omar; Fink, Jeffrey C.; Klassen, David K.; Drachenberg, Rene C.; Wiland, Anne; Wali, Ravinder K.; Cangro, Charles B.; Schweitzer, Eugene J.; Bartlett, Stephen T.; Weir, Matthew R.

doi:10.1097/01.asn.0000023435.07320.81

Cited by 401 publications

(419 citation statements)

References 30 publications

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“…Although still a poorly understood infection, several recent studies have shed light on the clinical aspects of BK allograft nephritis (25,26). Specific functional and molecular studies on the biological behavior of BK virus at the cellular level are not available, and very little is known about the interactions between the virus and the host cells.…”

Section: Discussionmentioning

confidence: 99%

BK Polyoma Virus Allograft Nephropathy: Ultrastructural Features from Viral Cell Entry to Lysis

Drachenberg¹,

Papadimitriou²,

Wali³

et al. 2003

American Journal of Transplantation

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BK virions must enter the host cell and target their genome to the nucleus in order to complete their life cycle. The mechanisms by which the virions accomplish these tasks are not known. In this morphological study we found that BK virions localized beneath the host cell cytoplasmic membrane in 60-70-nm, smooth (non-coated) monopinocytotic vesicles similar to, or consistent with, caveolae. In the cytoplasm, the monopinocytotic vesicles carrying virions appeared to fuse with a system of smooth, vesicles and tubules that communicated with the rough endoplasmic reticulum and was continuous with the Golgi system. Membrane-bound single virions and large tubuloreticular complexes loaded with virions accumulated in paranuclear locations. Occasional nuclei displayed virions within the perinuclear cisterna in association to the perinuclear viral accumulations. Tubular cells with mature productive infection had large nuclei, distended by daughter virions, whereas they lacked significant numbers of cytoplasmic virions. In addition to virally induced cell necrosis, there was extensive tubular cell damage (apoptosis and necrosis) in morphologically non-infected tubules. The observed ultrastructural interactions between the BK virions and host cells are remarkably similar to viral cell entry and nuclear targeting described for SV40 virus.

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Section: Discussionmentioning

confidence: 99%

BK Polyoma Virus Allograft Nephropathy: Ultrastructural Features from Viral Cell Entry to Lysis

Drachenberg¹,

Papadimitriou²,

Wali³

et al. 2003

American Journal of Transplantation

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“…When the disease is due to secondary reactivation, it can manifest as ureteric stenosis, retinitis, meningoencephalitis, and desquamative interstitial pneumonia, as well as the usual presentation of tubulointerstitial nephritis [11,12]. Because the seroprevalence in North America is high, BK viral reactivation is seen more commonly than primary infection [13]. This usually presents in the first year after transplantation, though rarely cases have been reported as late as 5 years [14].…”

Section: Bk Virus Can Cause Primary Infection As Well As Reactivationmentioning

confidence: 99%

Late-Onset BK Viral Nephropathy in a Kidney Transplant Recipient

Mathew

Holanda

Figanbaum

et al. 2014

Transplantation Proceedings

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“…The re-emergence of polyomavirus allograft nephropathy (PVAN) has been amply documented in many centers (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15). The specific factors that influence outcome are not known, but graft loss has been attributed to a late diagnosis of PVAN in kidneys already showing irreversible tissue damage (scarring) (7).…”

Section: Introductionmentioning

confidence: 99%

“…Performance of a renal biopsy is usually prompted by graft dysfunction, but more recently persistent PV viruria or viremia were suggested as appropriate indications (8,14,16).…”

Section: Introductionmentioning

confidence: 99%