 CMV is the most common viral infection after solid organ transplantation SOT and is associated with significant morbidity1. Without prophylaxis, most CMV disease occurs in the first 3 months post-transplant during the period of intense of immunosuppresion.2 SOT recipients at the greatest risk are those that are seronegative recipients of organs from seropositive donors CMV DR-.3, 4 Antiviral agents have proven to be useful in the prevention of CMV infection and disease in SOT recipients, including the high-risk DR- patients.5-9 Upon completion of prophylaxis however, CMV infection and disease occurs in about 50 and 25-30 respectively of DR- SOT recipients within the first year after transplant 30 rate of investigator treated CMV disease in PV16000.9 The incidence of CMV infection following prophylaxis in DR- lung transplant recipients may be as high as 80.10 As CMV disease occurring after prophylaxis will continue to impact morbidity and mortality in SOT recipients, it would be desirable to be able to predict which patient will develop this complication. Currently, there are no reliable methods that are routinely available to predict the risk of CMV infection or disease in an individual patient. CMV viral load testing after prophylaxis in DR- patients has been shown to have poor predictive value for subsequent CMV disease.11 CMV serology a measure of humoral immunity was also shown to be only of marginal use in predicting the risk of late onset disease.12 Cell mediated immunity CMI is known to be more important than humoral immunity in controlling CMV infection. CMV infection elicits a strong virus specific CD4 and CD8 T-cell response. CD8 T-cell responses to the virus often contain multiple antigen-specific reactivities including to viral pp65 or IE-1 antigens as well as pp50, glycoprotein B, and IE-2 and other antigens.13 CD4 T cells also play a part in CMV control via promotion of priming, expansion and maintenance of CD8 CMV-specific CTLs.14 Measuring an individuals CMI response to CMV may be a useful predictor of the risk of CMV infection or disease after prophylaxis. Patients with a poor CMI response especially a poor CD8 T-cell response could then be targeted with longer courses of antiviral prophylaxis. 