The human betaherpesviruses are cytomegalovirus (CMV), and the closely related human herpesviruses 6 and 7 (HHV-6 and HHV-7, respectively). For many years, CMV has been acknowledged to be a pathogen in transplant recipients causing direct effects (those concerned with organ involvement) and indirect effects (such as immunosuppression, atherosclerosis and graft rejection).¹ I will first summarize our improving understanding of the natural history of CMV infection, particularly the insight provided by quantitative measures of viral load.² I will then summarize all of the prospective studies that have been performed for HHV-6 and HHV-7 following solid organ and bone marrow transplantation. Although individual case reports have appeared associating HHV-6 with pneumonitis, encephalitis and bone-marrow failure, an overview of these cohort studies suggests that these events are rare. Instead, emerging data indicate that the main effects of these viruses may be indirect, in particular by triggering graft rejection. The possible pathogenic mechanisms and treatment implications of this observation will be discussed.

1. Rubin RH. The indirect effects of cytomegalovirus infection on the outcome of organ transplantation. JAMA 1989;261:3607-3609.

2. Cope AV, Sabin C, Burroughs A et al. Interrelationships among quantity of human cytomegalovirus (HCMV) DNA in blood, donor-recipient serostatus, and administration of methylprednisolone as risk factors for HCMV disease following liver transplantation. J Infect Dis 1997;176:1484-1490.