Longitudinal study of BK virus infection in adult allogeneic haematopoietic stem cell transplant

Abstract number: P1218

Corneille J., Dhédin N., Deback C., Uzunov M., Nguyen S., Vernant J., Agut H., Boutolleau D.

Objectives: In haematopoietic stem cell transplant (HSCT) recipients, BK virus (BKV) infection is associated with haemorrhagic cystitis (HC) occurring after engraftment. Nevertheless, no virological marker of late-onset HC has been clearly identified. The aim of this longitudinal study was to determine the incidence and the risk factors of BKV infection in HSCT recipients, to analyse the association of BKV load in whole blood with HC, and to evaluate whether systematic follow-up of BKV infection is warranted.

Methods: BKV load was measured retrospectively using a real-time PCR assay in whole blood specimens from 61 consecutive allogeneic HSCT recipients (38 men, 23 women, median age: 45 years) collected at 0, 1, 2, 3, 6, 9, and 12 months post-transplantation.

Results: Fifteen patients (25%) developed BKV viraemia at a median of 2 months (1–3) after transplantation. Acute leukaemia as underlying disease was identified as a risk factor for BKV infection (P = 0.03). BKV infection was associated with acute graft-versus-host disease (P = 0.003) and haematuria (P < 0.001). The maximum BKV load was higher in patients with haematuria than in those without haematuria (median, 1685 vs. 160 copies/mL; P = 0.05). The occurrence of haematuria was statistically associated with a concomitant BKV load >500 copies/mL (P = 0.04) and with BKV detection in at least two consecutive blood specimens (P = 0.04). Lymphocyte recovery in patients with haematuria was delayed compared to those without haematuria. Ten patients (16%) experienced both BKV and cytomegalovirus (CMV) infections after transplantation. In all cases, CMV infection appeared either before (n = 5) or concomitantly (n = 5) with BKV infection. Overall, the frequency of BKV detection was statistically higher in CMV-positive samples than in CMV-negative samples (22% vs. 5%; P < 0.001). No adenovirus infection was evidenced in patients with haematuria.

Conclusion: BKV viraemia is highly associated with the occurrence of HC in HSCT recipients. Prolonged BKV viraemia and BKV load over 500 copies/mL of whole blood were identified as predictive markers for the development HC. The analysis of BKV load kinetics and lymphocyte recovery after transplantation underlines the potential role of cellular immunity in the pathogenesis of HC. Our results suggest a possible role of CMV in the process of BKV infection. The monitoring of BKV load appears useful to identify HSCT recipients at risk for developing post-engraftment HC.

Session Details

Date: 10/04/2010
Time: 00:00-00:00
Session name: Abstracts 20th European Congress of Clinical Microbiology and Infectious Diseases
Location: Vienna, Austria, 10 - 13 April 2010
Presentation type:
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