Abstract 2795: Parvovirus B19 in the Myocardium of Pediatric Cardiac Transplant Patients is Associated With Transplant Coronary Artery Disease
Background: The presence of parvovirus B19 genome in the myocardium of cardiac transplant patients has been increasingly reported in the literature. Cellular rejection and transplant coronary artery disease (TCAD) are important processes that decrease transplant graft survival. The implications of parvovirus B19 in these processes and its effect on transplant graft survival are unknown.
Hypothesis: Parvovirus B19 in the myocardium negatively affects transplant graft survival via cellular rejection or other mechanisms.
Methods: From 9/2002 to 12/2005 surveillance endomyocardial biopsies were evaluated for the presence of viral genome. Quantitative RT-PCR was performed on parvovirus positive biopsies to correlate viral copy number to cellular rejection. ISHLT cellular rejection scores of parvovirus positive and negative biopsies were compared. All parvovirus B19 genomes amplified were sequenced to identify parvovirus type. Freedom from advanced TCAD was assessed with Kaplan-Meier analysis and log rank.
Results: Seven hundred biopsies were evaluated; 121 were positive for viral genome, of which 100 (82.6%) were positive for parvovirus B19 (7 were positive for parvovirus B19 and EBV). Thirty-two parvovirus positive biopsies were available for qRT-PCR analysis. Higher viral copy number/ng of DNA did not correlate with rejection score. Parvovirus B19 amplicons were genotyped as type 1 in all cases. Children with persistent parvovirus B19 infection, for greater than 6 months (n=20), were predisposed to early development of advanced TCAD (p < 0.001).
Conclusions: Cellular rejection does not correlate with the presence or quantity of parvovirus B19 genome in the myocardium. However, children with chronic parvovirus B19 infection are at increased risk of earlier TCAD, supporting the hypothesis that parvovirus B19 negatively affects graft survival.