edoc

BK virus large T and VP-1 expression in infected human renal allografts

Seemayer, C. A. and Seemayer, N. H. and Dürmüller, U. and Gudat, F. and Schaub, S. and Hirsch, H. H. and Mihatsch, M. J.. (2008) BK virus large T and VP-1 expression in infected human renal allografts. Nephrology, dialysis, transplantation, Vol. 23, H. 12. pp. 3752-3761.

Full text not available from this repository.

Official URL: http://edoc.unibas.ch/dok/A6008121

Downloads: Statistics Overview

Abstract

OBJECTIVE: We investigated the expression of early and late phase BK virus (BKV) proteins and their interactions with host cell proteins in renal allografts, with ongoing polyomavirus associated nephropathy (PVAN), and correlated this with the nuclear and cell morphology. METHODS: Frozen sections from three patients with renal allografts (two biopsies, one explant) with PVAN were analysed by indirect immunofluorescence using BKV specific anti-polyoma large T-antigen and anti-VP-1 antibodies, as well as anti-p53, anti-Ki67, anti-caspase-3, anti-bcl2 and anti-cytokeratin 22 antibodies. Nuclear morphology and size were estimated by DNA Hoechst staining. RESULTS: In infected tubular cells the early and late phases of infection could be distinguished according to expression of large T-antigen or VP-1. The early phase revealed almost normal nuclear proportions, whereas in later phases nuclear size increased about 2 to 3 fold. Expression of large T-antigen was strongly associated with accumulation of p53 in the nucleus, accompanied by the activation of the cell cycle associated cell protein Ki67. In contrast, expression of BKV VP1 correlated only weakly with p53. Virus dependent cell lysis was due to necrosis, since neither caspase 3 nor nuclear nor cytoskeleton changes indicated apoptosis. CONCLUSION: In our selected patients with PVAN a clear distinction between early and late phases was possible, according to the protein expression patterns of BKV markers. Striking nuclear enlargement is only present in the late phase of infection. In the inflammatory setting of PVAN, BKV dependent effects appear to be mediated by the inhibition of p53, resulting in the activation of the cell cycle. We assume that in PVAN similar BKV mechanisms are operative as in certain in vitro systems.
Faculties and Departments:03 Faculty of Medicine > Bereich Querschnittsfächer (Klinik) > Pathologie USB
03 Faculty of Medicine > Departement Klinische Forschung > Bereich Querschnittsfächer (Klinik) > Pathologie USB
03 Faculty of Medicine > Bereich Medizinische Fächer (Klinik) > Nephrologie > Transplantationsimmunologie und Nephrologie (Steiger)
03 Faculty of Medicine > Departement Klinische Forschung > Bereich Medizinische Fächer (Klinik) > Nephrologie > Transplantationsimmunologie und Nephrologie (Steiger)
03 Faculty of Medicine > Departement Biomedizin > Division of Medical Microbiology > Transplantation Virology (Hirsch)
UniBasel Contributors:Mihatsch, Michael J. and Hirsch, Hans H. and Seemayer, Christian A. and Schaub, Stefan
Item Type:Article
Article Subtype:Further Journal Contribution
Bibsysno:Link to catalogue
Publisher:Oxford University Press
ISSN:0931-0509
Note:Publication type according to Uni Basel Research Database: Journal item
Related URLs:
Identification Number:
Last Modified:20 Jun 2014 07:55
Deposited On:20 Jun 2014 07:55

Repository Staff Only: item control page