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Molecular evaluation of BK polyomavirus nephropathy.

Publication ,  Journal Article
Mannon, RB; Hoffmann, SC; Kampen, RL; Cheng, OC; Kleiner, DE; Ryschkewitsch, C; Curfman, B; Major, E; Hale, DA; Kirk, AD
Published in: Am J Transplant
December 2005

Understanding at a molecular level, the immunologic response of polyomavirus nephropathy (PVN), a critical cause of kidney graft loss, could lead to new targets for treatment and diagnosis. We undertook a transcriptional evaluation of kidney allograft biopsies from recipients with PVN or acute rejection (AR), as well as from recipients with stable allograft function (SF). In both the PVN and AR groups, Banff histologic scores and immunohistochemical analysis of inflammatory infiltrates were similar. Despite their different etiologies, the transcriptional profiles of PVN and AR were remarkably similar. However, transcription of genes previously linked to AR including CD8 (65.9 +/- 18.8) and related molecules IFN-gamma(55.1 +/- 17.0), CXCR3 (49.9 +/- 12.8) and perforin (153.8 +/- 50.4) were significantly higher in PVN compared to AR (30.9 +/- 2.0, 14.0 +/- 7.3, 12.1 +/- 7.3 and 15.6 +/- 3.8-fold, respectively; p < 0.01). Importantly, transcription of molecules associated with graft fibrosis including matrix collagens, TGFbeta, MMP2 and 9, as well as markers of epithelial-mesenchymal transformation (EMT) were significantly higher in PVN than AR. Thus, renal allografts with PVN transcribe proinflammatory genes equal in character and larger in magnitude to that seen during acute cellular rejection. BK infection creates a transcriptional microenvironment that promotes graft fibrosis. These findings provide new insights into the intrarenal inflammation of BK infection that promotes graft loss.

Duke Scholars

Published In

Am J Transplant

DOI

ISSN

1600-6135

Publication Date

December 2005

Volume

5

Issue

12

Start / End Page

2883 / 2893

Location

United States

Related Subject Headings

  • Viral Load
  • Tumor Virus Infections
  • Transplantation, Homologous
  • Transcription, Genetic
  • Surgery
  • Postoperative Complications
  • Polyomavirus Infections
  • Middle Aged
  • Male
  • Kidney Transplantation
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Mannon, R. B., Hoffmann, S. C., Kampen, R. L., Cheng, O. C., Kleiner, D. E., Ryschkewitsch, C., … Kirk, A. D. (2005). Molecular evaluation of BK polyomavirus nephropathy. Am J Transplant, 5(12), 2883–2893. https://doi.org/10.1111/j.1600-6143.2005.01096.x
Mannon, R. B., S. C. Hoffmann, R. L. Kampen, O. C. Cheng, D. E. Kleiner, C. Ryschkewitsch, B. Curfman, E. Major, D. A. Hale, and A. D. Kirk. “Molecular evaluation of BK polyomavirus nephropathy.Am J Transplant 5, no. 12 (December 2005): 2883–93. https://doi.org/10.1111/j.1600-6143.2005.01096.x.
Mannon RB, Hoffmann SC, Kampen RL, Cheng OC, Kleiner DE, Ryschkewitsch C, et al. Molecular evaluation of BK polyomavirus nephropathy. Am J Transplant. 2005 Dec;5(12):2883–93.
Mannon, R. B., et al. “Molecular evaluation of BK polyomavirus nephropathy.Am J Transplant, vol. 5, no. 12, Dec. 2005, pp. 2883–93. Pubmed, doi:10.1111/j.1600-6143.2005.01096.x.
Mannon RB, Hoffmann SC, Kampen RL, Cheng OC, Kleiner DE, Ryschkewitsch C, Curfman B, Major E, Hale DA, Kirk AD. Molecular evaluation of BK polyomavirus nephropathy. Am J Transplant. 2005 Dec;5(12):2883–2893.
Journal cover image

Published In

Am J Transplant

DOI

ISSN

1600-6135

Publication Date

December 2005

Volume

5

Issue

12

Start / End Page

2883 / 2893

Location

United States

Related Subject Headings

  • Viral Load
  • Tumor Virus Infections
  • Transplantation, Homologous
  • Transcription, Genetic
  • Surgery
  • Postoperative Complications
  • Polyomavirus Infections
  • Middle Aged
  • Male
  • Kidney Transplantation