The pathogenesis of CMV reactivation, viral replication, disease progression, and viral persistence is likely related to a number of host factors in transplant patients, including degree and type of immunosuppressive therapy, and pre-existing immunity [8,9]. However, CMV is a remarkably complex virus with a large genome encoding approximately 200 open reading frames. A number of viral factors likely also play a role in determining the risk of CMV disease, the risk of tissue invasion, the response to therapy, and the risk of recurrence once therapy is initiated. The virus commits a large percentage of its total genome coding capacity to the tasks of modulating host cell behaviour and host response to infection [8,9]. These include CMV gene products aimed at escaping host defence mechanisms which are commonly referred to as CMV immune evasion genes [9-11]. Some of these immune evasion genes encode for proteins that can actively interfere with distinct steps in the antigen expression pathway and thus contribute to viral persistence despite an active host immune response. For example US2, US3, US6, and US11 encode for a protein whose ultimate effect is to reduce the levels of MHC class I proteins on the surface of infected cells. The CMV UL141 gene product provides protection against killing by a wide array of NK cell populations, via blocking of surface expression of NK cell-activating ligand CD155 [26]. Also, human CMV expresses several homologues of host G protein-coupled receptors (GPCRs), of which the chemokine receptor homologue US28 is the best characterized [27]. Although the exact significance of US28 has not been determined, the protein product may play a role in cell entry, leukocyte chemotaxis, viral dissemination and immune evasion [27].