In the present study we found that 38% (10 individuals) of the graft recipients developed HHV-6 infection ( Table 1) . Eight patients (30%) had detectable viral DNA levels in two or more samples in subsequent tests during the six weeks following SCT and another two (8%) had a single sample positive at a later time. It is likely that the HHV-6 infection that occurred after transplantation was due to activation of the virus in the bodies of the recipients, since most of the recipients were immune to HHV-6 and no virus was found before SCT. However, we do not know whether HHV-6 strains detected in the present study were derived from the donor or were transfered from other sources to the seronegative recipients. The virus probably remains latent in the body after primary infection, as do other human herpesviruses. If the HHV-6 was derived from the donor, it must have been latently infecting the donor's hemopoietic stem cells and was activated to replicate after transfer to the recipient. In other cases, the virus was probably reactivated from the recipient's own body by factors such as a profound immune dysfunction or an allogeneic reaction after transplantation.