Human polyoma virus in renal allograft biopsies: Morphological findings and correlation with urine cytology

Drachenberg, Cinthia B.; Beskow, Christian O.; Cangro, Charles B.; Bourquin, Patricia M.; Simsir, Aylin; Fink, Jeffrey C.; Weir, Matthew R.; Klassen, David K.; Bartlett, Stephen T.

doi:10.1016/s0046-8177(99)90252-6

Cited by 244 publications

(204 citation statements)

References 24 publications

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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%

Histological Patterns of Polyomavirus Nephropathy: Correlation with Graft Outcome and Viral Load

Drachenberg¹,

Papadimitriou²,

Hirsch

et al. 2004

American Journal of Transplantation

362

390

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Section: Introductionmentioning

confidence: 99%

Histological Patterns of Polyomavirus Nephropathy: Correlation with Graft Outcome and Viral Load

Drachenberg¹,

Papadimitriou²,

Hirsch

et al. 2004

American Journal of Transplantation

362

390

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“…Both can transform cells in culture and cause cancer in animals (1,2) and are highly homologous to the human BK and JC polyomaviruses (BKV and JCV, respectively). In the context of an impaired immune system, BKV and JCV infection can lead to kidney transplant loss or progressive multifocal leukoencephalopathy (3,4). SV40 serves as a paradigm for cholesterol-dependent endocytosis and as a useful vector for gene transfer into eukaryotic cells.…”

mentioning

confidence: 99%

Structural basis of GM1 ganglioside recognition by simian virus 40

Neu

Woellner

Gauglitz

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

169

230

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Simian virus 40 (SV40) has been a paradigm for understanding attachment and entry of nonenveloped viruses, viral DNA replication, and virus assembly, as well as for endocytosis pathways associated with caveolin and cholesterol. We find by glycan array screening that SV40 recognizes its ganglioside receptor GM1 with a quite narrow specificity, but isothermal titration calorimetry shows that individual binding sites have a relatively low affinity, with a millimolar dissociation constant. The high-resolution crystal structure of recombinantly produced SV40 capsid protein, VP1, in complex with the carbohydrate portion of GM1, reveals that the receptor is bound in a shallow solvent-exposed groove at the outer surface of the capsid. Through a complex network of interactions, VP1 recognizes a conformation of GM1 that is the dominant one in solution. Analysis of contacts provides a structural basis for the observed specificity and suggests binding mechanisms for additional physiologically relevant GM1 variants. Comparison with murine Polyomavirus (Polyoma) receptor complexes reveals that SV40 uses a different mechanism of sialic acid binding, which has implications for receptor binding of human polyomaviruses. The SV40 -GM1 complex reveals a parallel to cholera toxin, which uses a similar cell entry pathway and binds GM1 in the same conformation.crystal structure ͉ glycan array ͉ polyomaviruses ͉ viral attachment ͉ protein-carbohydrate complex

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“…Tissue damage results from a combination of direct viral cytolytic effects and secondary inflammatory responses. The latter may be immune specific or nonspecific in nature (7,8). The intricate interactions between the virus and the immune system lead to various clinicopathologic forms of BK disease, as has been schematized previously by Hirsch (9).…”

Section: Spectrum Of Clinicopathologic Manifestationsmentioning

confidence: 94%

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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Human polyoma virus in renal allograft biopsies: Morphological findings and correlation with urine cytology

Cited by 244 publications

References 24 publications

Histological Patterns of Polyomavirus Nephropathy: Correlation with Graft Outcome and Viral Load

Histological Patterns of Polyomavirus Nephropathy: Correlation with Graft Outcome and Viral Load

Structural basis of GM1 ganglioside recognition by simian virus 40

Histologic versus Molecular Diagnosis of BK Polyomavirus–Associated Nephropathy

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