Cytomegalovirus-associated allograft rejection in heart transplant patients.
OBJECTIVE
Modern antiviral strategies are effective in controlling the clinical syndromes associated with acute cytomegalovirus infection in heart transplant recipients. Despite this effectiveness, subclinical cytomegalovirus infection is a common finding in these patients and its impact on long-term graft outcome is currently underestimated.


RESULTS
Recent studies provide evidence implicating subclinical cytomegalovirus infection in the pathogenesis of allograft rejection and cardiac allograft vasculopathy. In this process, cytomegalovirus interacts with local inflammatory pathways, and systemic immune-regulation mechanisms, which may lead to graft damage, even in the absence of cytomegalovirus replication within the graft. Consequently, in addition to pharmacologic strategies that inhibit viral replication, immune-based therapies that abrogate host immune response may provide an effective tool to prevent the indirect impact of cytomegalovirus on graft function.


CONCLUSIONS
Current evidence suggests that subclinical cytomegalovirus infection plays an important role in the pathogenesis of long-term graft dysfunction in heart transplant recipients and in other solid organ transplant recipients. Pending the availability of definitive data from randomized trials, we propose that the use of pharmacologic and immune-based approaches, directed at complete suppression of cytomegalovirus infection, represents the best strategy for prevention of cytomegalovirus-induced rejection, cardiac allograft vasculopathy and chronic allograft damage.
Potena
Luciano
L
Institute of Cardiology, University of Bologna, Bologna, Italy.
Valantine
Hannah A
HA
D003587:Cytomegalovirus / Q000472:pathogenicity; D003586:Cytomegalovirus Infections / Q000150:complications / Q000188:drug therapy / Q000276:immunology* / Q000821:virology*; D006084:Graft Rejection / Q000209:etiology* / Q000517:prevention & control; D016027:Heart Transplantation; D006801:Humans; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism; D011183:Postoperative Complications / Q000188:drug therapy / Q000276:immunology / Q000821:virology
D018836:Inflammation Mediators