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Title: Epstein-Barr virus infection in cardiothoracic transplant recipients
Author: Hopwood, Paul A.
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 2001
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Epstein-Barr virus (EBV) is a human DNA herpesvirus which establishes a persistent latent infection in vivo in B-lymphocytes. Iatrogenic immunosuppression to prevent rejection of transplanted organs predisposes to EBV positive post-transplant B-lymphoproliferative disease (PTLD). This study followed 96 adult cardiothoracic transplant recipients for up to 1110 days (mean follow up time of 415 days) post-transplant. Blood samples were taken immediately prior to transplant surgery and multiple samples taken at intervals following transplantation (1 to 14 samples per patient, mean of 5 samples). Blood samples were also obtained from normal EBV seropositive individuals and patients with infectious mononucleosis and PTLD. EBV load in peripheral blood mononuclear cells (PBMs) were determined in each sample using a semi-quantitative DNA PCR capable of detecting 1-10 EBV genomes in a total of 106 cells. RT-PCRs were developed to examine whether the pattern of EBV gene expression changed following transplantation due to immunosuppressive therapy and how these changes relate to PTLD development. The results show that post-transplant EBV load significantly increases above that detected in normal EBV seropositives (EBV load in normals ranged from <1 to 200 EBV genomes/ 106 PBMs, median of 10 EBV genomes/ 106 PBMs) in 52% of transplant recipients and reaches levels equivalent to that detected in patients with clinically apparent EBV associated disease (IM or PLTD) in 19%. EBV load pre-transplant in all patients was equivalent to that in normal EBV seropositives (p>0.05). Thus high EBV load is associated with, but not diagnostic of EBV associated disease. EBV gene expression prior to transplantation did not vary from that in normal EBV seropositives, with detection of LMP2a in 20/36 subjects and LMP2a and 2b in 3/36 but no detection of lytic transcripts (gp350) or EBNA3C. In IM, latency III was detected (EBNA3C) in 2/28 subjects, latency III and lytic replication in 4/28 and restricted latency with lytic replication in 5/28.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available