Infection with HCMV in healthy individuals generally results in mild or subclinical illness. Pathogenic infections occur predominantly in immunodeficient patients, such as transplant recipients, neonates and patients with AIDS. Primary infection is frequently latent or chronic and PBLs represent sites for virus latency and persistence. HCMV can be recovered from PMNL, monocytes and T-lymphocytes. Although virus-related cases of haematopoietic dysfunction are seen infrequently in infected normal persons, the importance of HCMV as a pathogenic agent in haematopoiesis is dramatically illustrated in the case of patients receiving BMT. Primary or reactivated HCMV infections are a common feature in BMT recipients, enhancing failure of marrow engraftment, GVHD, and many opportunistic infections. HCMV can infect both haematopoietic progenitor cells and stromal elements, identifying the entire haematopoietic system as a target for HCMV dissemination and latency. As a result, lympho- and myelosuppression can be due to both direct inhibition of progenitor cell growth as well as the failure of stem cell self-renewal due to stromal cell dysfunction. HCMV can also exert suppressive effects on immune cell function by direct and indirect mechanisms. These effects can have dire consequences, particularly when a state of immunosuppression already exists, as in the HIV infection. The diverse effects of CMV on the lymphohaematopoietic system are summarized in Figure 1.