The Epstein–Barr virus DNA load in the peripheral blood of transplant recipients does not accurately reflect the burden of infected cells

Susanne Fink, Ming Han Tsai, Paul Schnitzler, Martin Zeier, Peter Dreger, Patrick Wuchter, Olcay C. Bulut, Uta Behrends, Henri Jacques Delecluse*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

Transplant recipients frequently exhibit an increased Epstein–Barr virus (EBV) load in the peripheral blood. Here, we quantitated the EBV-infected cells in the peripheral blood of these patients and defined the mode of viral infection, latent or lytic. These data indicated that there is no strong correlation between the number of infected cells and the EBV load (EBVL). This can be explained by a highly variable number of EBV copies per infected cell and by lytic replication in some cells. The plasma of these patients did not contain any free infectious viruses, but contained nevertheless EBV DNA, sometimes in large amounts, that probably originates from cell debris and contributed to the total EBVL. Some of the investigated samples carried a highly variable number of infected cells in active latency, characterized by an expression of the Epstein–Barr nuclear antigens (EBNA2) protein. However, a third of the samples expressed neither EBNA2 nor lytic proteins. Patients with an increased EBVL represent a heterogeneous group of patients whose infection cannot be characterized by this method alone. Precise characterization of the origin of an increased EBVL, in particular, in terms of the number of EBV-infected cells, requires additional investigations including the number of EBV-encoded small RNA-positive cells.

Original languageEnglish
Pages (from-to)57-67
Number of pages11
JournalTransplant International
Volume30
Issue number1
DOIs
StatePublished - 1 Jan 2017

Keywords

  • Epstein-Barr virus infection
  • malignancies and long term compliations after transplantation
  • post-transplant lymphoproliferative disorders

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