Cytomegalovirus (CMV) is the most important pathogen affecting organ transplant recipients. It is a member of the genus Herpisvirus. Table 1 Symptomatic infection occurs in 20-60% of all transplant recipients, depending on the intensity of IS used and the diagnostic tests used to make the diagnosis. In a study at the NKTI by Mendoza et al on the causes of infections requiring hospitalization among 125 kidney transplants performed from 1996-1999 using mycophenolate mofetil, 42% developed infections in the first year post transplant.1 CMV accounted for 42% of all viral infections, with the incidence of viral infections equivalent to that of bacterial infections in the first 3 months post-transplant at 45%. Viral disease decreased after 3months and bacterial infections predominated up to the first year. In another retrospective review of 1126 kidney transplants, 9% of kidney recipients experienced symptomatic CMV infection.2 CMV infection is present if one or more is found: seroconversion with the appearance of anti-CMV IgM antibodies; a fourfold increase in pre-existing antiCMV IgG titers; detection of CMV antigens in infected blood cells; and/or isolation of the virus by culture of the throat, buffy coat, or urine. CMV disease, on the other hand, requires clinical signs and symptoms, such as fever, leucopenia, or organ involvement. CMV infection results through the transmission of CMV via the seropositive donor kidney to a seronegative recipient (D+/R-) resulting in primary infection, from reactivation of CMV in a seropositive recipient (D-/R+) due to IS, and finally, a seropositive recipient may acquire a super infection from a CMV positive donor (D+/ R+). In the study by Mendoza et al, Filipinos were 99% seropositive for antibody, so that CMV infection results mainly from the 2 latter means in our setting.1 Although most studies concentrated on the prevention of primary infection (D+/R-), analyses of data from the USRDS and UNOS revealed that by 3 years it is D+/R+ group, and not the D+/R- group that has the worst graft and patient survival.3,4 This may be due to the double CMV exposure with reactivation of differing latent donor and recipient CMV. CMV can also predispose to acute rejection by various effects such as upregulating the transcription and expression of IL-2 and the IL2R and preventing the inhibitory effect of cyclosporine on IL-2 gene transcription among others. It has also been associated with chronic rejection and atherosclerosis. CMV may affect the renal graft directly, resulting in tissue injury and clinical disease, and indirectly through cytokines and chemokines produced in response to CMV replication. The immunomodulatory effects of CMV result in an increased risk for opportunistic infections. The clinical manifestations vary from mild asymptomatic disease to severe fatal disease. Common sites of disease include the lungs, gastrointestine tract, biliary tract, and pancreas. CMV disease manifests with fever, leucopenia and elevated transaminases. Pneumonitis can be very severe with dyspnea, hypoxia and interstitial infiltrates. The usual cause of death in CMV infection is severe pneumonitis.