Human herpesvirus 6 infection after living related liver transplantation

Abstract

The aim of the study was to investigate human herpesvirus-6 (HHV-6) infection after liver transplantation from living related donors, and to evaluate the reliability of the presence of HHV-6 DNA in plasma by the polymerase chain reaction (PCR) for monitoring active HHV-6 infection. EDTA peripheral blood was collected from 47 donor and recipient (16 males and 31 females, age 1–320 months) pairs at the time of transplantation and biweekly from these recipients after transplantation until 2 months after operation. Isolation of HHV-6 and serological assays were carried out to evaluate active HHV-6 infection in this study. The presence of the viral DNA in plasma was tested by nested PCR. Four clinical events, such as unexplained fever, thrombocytopenia, rejection, and central nervous system (CNS) involvement, were evaluated for clinical features of the virus infection. Risk factors for the virus activity after liver transplantation were also examined. HHV-6 activity was detected in 23 (49%) of the 47 recipients approximately 2–4 weeks after transplantation. All 9 isolates were HHV-6 variant B. The presence of the viral DNA in plasma correlated well with virus isolation and serology (P < 0.01). Only unexplained fever was associated statistically with HHV-6 activity after liver transplantation (P < 0.01). If the recipient was seronegative to HHV-6 before transplantation, the recipient was more likely to develop the active virus infection after liver transplantation (P = 0.11). HHV-6 activity occurred in one-half of the recipients approximately 2–4 weeks after liver transplantation, and there was a close association between HHV-6 activity and unexplained fever following transplantation. Detection of the viral DNA in plasma by PCR is useful for monitoring active HHV-6 infection in these patients. Seronegative recipients were more likely to have evidence of active HHV-6 infection after liver transplantation. J. Med. Virol. 62:52–59, 2000. © 2000 Wiley-Liss, Inc.