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1 January 2006

Volume 193, Number 1
The Journal of Infectious Diseases 2006;193:80–87
© 2005 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2006/19301-0013$15.00
DOI: 10.1086/498530
MAJOR ARTICLE

Rapid Dynamics of Polyomavirus Type BK in Renal Transplant Recipients

Georg A. Funk,1,2

Jürg Steiger,3 and

Hans H. Hirsch2,4

1School of Biological Sciences, Royal Holloway University of London, Egham, United Kingdom; 2Transplantation Virology, Medical Microbiology, Department of Clinical and Biological Sciences, University of Basel, and 3Transplantation Immunology and Nephrology and 4Infectious Diseases and Hospital Epidemiology, University Hospitals Basel, Basel, Switzerland

Background.Polyomavirus type BK–associated nephropathy (PVAN) is an emerging cause of early renal transplant failure. No specific antiviral treatment has been established. Current interventions rely on improving immune functions by reducing immunosuppression. In patients with PVAN, a high BK virus (BKV) load is detectable in plasma. However, the relationship between BKV replication and disease is not well understood.

Methods.In a retrospective analysis of BKV plasma load in renal transplant recipients undergoing allograft nephrectomy ( ) or changes in immunosuppressive regimen ( ), we calculated viral clearance rates and generation times and estimated the loss of BKV‐infected renal cells.

Results.After nephrectomy, BKV clearance was fast (viral half‐life [t1/2], 1–2 h) or moderately fast (t1/2, 20–38 h), depending on the sampling density, but it was independent of continued immunosuppressive regimens. After changing immunosuppressive regimens, BKV was cleared with a t1/2 of 6 h–17 days. Using the basic reproductive ratio, the efficacies of intervention ranged from 7% to 83% (mean, 28%; median, 22%).

Conclusion.The results emphasize that high‐level BKV replication is a major pathogenetic factor that may have implications for genome rearrangements, immune evasion, and antiviral resistance.

Received 5 April 2005; accepted 18 July 2005; electronically published 30 November 2005.

Reprints or correspondence: Pr. Hans H. Hirsch, Transplantation Virology, Medical Microbiology, Dept. of Clinical and Biological Sciences, University of Basel, Petersplatz 10, CH‐4003 Basel, Switzerland ().

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Ellen Krautkrämer, Theresa M. Klein, C. Sommerer, Paul Schnitzler, Martin Zeier. (2009) Mutations in the BC-loop of the BKV VP1 region do not influence viral load in renal transplant patients. Journal of Medical Virology 81:1, 75-81
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E. Ramos, H.H. Hirsch. (2006) Polyomavirus-associated nephropathy: updates on a persisting challenge. Transplant Infectious Disease 8:2, 59-61
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  • Potential conflicts of interest: none reported.

    Financial support: European Community (Marie Curie Fellowship, contract MEIF‐CT‐2004‐501039 to G.A.F.); Ausbildungsstiftung für den Kanton Schwyz und die Bezirke See und Gaster (grant to G.A.F.); Swiss National Fund (grant 3200‐062021.00 to H.H.H.).

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