Nearly 30 years have elapsed since Rowe and Weller and their colleagues 
discovered human cytomegalovirus (CMV). Because of its complex structure, long 
replicative cycle, low yield in vitro, and highly species-specific 
cell-substrate requirement, the cellular and molecular biologic analyses of 
human CMV have been slow, but recombinant DNA and monoclonal antibody 
technologies are bringing about rapid changes. Because of the long period of 
latency and wide range of disease presentations, epidemiologic and medical 
insights have also come slowly. However, the clinical events that occur during 
iatrogenic immunosuppression (transplantation and cancer therapy) and as a 
result of immunocompromise due to human immunodeficiency virus infection are 
currently promoting our understanding of the epidemiology of CMV disease and the 
definition of its clinical spectrum. Rapid diagnostic methods, antiviral drugs, 
and vaccines for CMV are becoming available. We may not yet understand 
completely the impact of this agent on the nonimmunosuppressed or aspects of its 
pathogenesis: e.g., the immune functions controlling recrudescence and the 
possibility of increased disease severity in those with no detectable immune 
defect. With the availability of new approaches, other issues should be 
clarified, such as the functions of host and virus involved in the mechanism of 
persistence.