Detection of viral genome in rejecting cardiac transplant patients has been reported, with coxsackievirus and adenovirus causing premature graft failure. Recently, parvovirus B19 (PVB19) genome in myocardial samples has been increasingly reported but its role in cardiac pathology and effect on transplant graft survival are unknown. The objectives were to determine if changes in the viruses identified in the myocardium represent an epidemiologic shift in viral myocardial disease and whether PVB19 adversely affects transplant graft survival.
From 9/2002 to 12/2005, 99 children (3 weeks-18 years) with heart transplants had endomyocardial biopsies evaluated for the presence of viral genome utilizing nested PCR. Cellular rejection was assessed by histology of biopsies, while transplant coronary artery disease (TCAD) was diagnosed by coronary angiography or histopathology.
Seven hundred biopsies were evaluated from 99 patients; 121 biopsies had viral genome with 100 (82.6%) positive for PVB19, 24 for Epstein-Barr virus (EBV; 7 positive for PVB19 and EBV), 3 for CMV and 1 for adenovirus. Presence of PVB19 genome did not correlate with rejection score, nor did higher viral copy number. Children with persistent PVB19 infection (>6 months; n=20), had early development of advanced TCAD (p<0.001).
PVB19 is currently the predominant virus detected in heart transplant surveillance biopsies, possibly representing an epidemiologic shift. While cellular rejection does not correlate with the presence or quantity of PVB19 genome in the myocardium, children with chronic PVB19 infection have increased risk for earlier TCAD, supporting the hypothesis that PVB19 negatively affects graft survival.