Herpesviruses persist throughout life after primary infection. Viral proliferation occurs either spontaneously or under conditions of immunosuppression. Reactivation can lead to illnesses that typically differ in their clinical presentation from the disease associated with the primary infection. After SCT, reactivating members of the β-herpesvirinae subfamily (among them HHV-6) frequently cause serious, sometimes life--threatening disease [8, 12] . HHV-6 infection or reactivation in these individuals has been associated with a delay or suppression of marrow engraftment [12] , pneumonia [2] , skin rash, and fever [16] . Although it is difficult to prove an etiologic association of the virus with these disease events, their propinquity with HHV-6 activity in the absence of other possible causes suggests that at the very least a subset of these events is due to HHV-6 activity.