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Viral infections remain among the most important challenges in the management of the transplant recipient. This observation reflects both a predisposition to viral infection by immunosuppression that targets T-cell function, the diverse population of viruses, and the impact of viruses including infection, graft rejection, and malignancies. Traditionally, the manifestations of cytomegalovirus (CMV) infection have been termed “direct” (organ-specific) and “indirect” (immune) effects. More accurate terms might be “viral cytopathic” effects and “cellular and systemic immunologic” effects. The clinical manifestations of viral CMV infections are the result of suppression of multiple host defense mechanisms, predisposing to secondary invasion by such pathogens as P. jiroveci, Candida and Aspergillus species and increasing the risk for graft loss and death. As the biology of viral infection is explored, many of these manifestations of viral infection appear to be mediated not only by T-cells but also by the innate immune system.