Management of cytomegalovirus infections in blood and marrow transplant recipients.

Abstract

As one of the 8 human herpes viruses (designated human herpes virus 5), CMV shares characteristics with other herpes viruses including virion and genome structure and the ability to establish lifelong persistent and latent infections after primary exposure.1 The basic biology and pathogenesis of CMV disease go beyond the scope of this overview and are reviewed elsewhere.1–4 CMV infection in immunocompromised individuals is acquired exogenously or results from reactivation of latent virus. Reactivation of latent endogenous virus appears to be the dominant mechanism of infection in immunocompromised patients. The frequency at which CMV in seropositive patients can be superinfected by exogenous CMV is uncertain, but co-infection with different strains can occur.5,6 In seronegative individuals, CMV is virtually always acquired from blood products or from transplanted organs.7 Transplant of an organ from a seropositive donor into a seronegative recipient results in a high risk of infection (80–90%), higher levels of CMV replication, and a higher incidence of disease than reactivation of latent virus.8 In contrast, transplantation of marrow or peripheral blood stem cells (PBSC) from a seropositive donor into a seronegative recipient results in CMV infection in only 20–25% of patients.9 The reasons for this difference are only poorly understood.