Editorial
Copyright ©2009 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Jun 7, 2009; 15(21): 2561-2569
Published online Jun 7, 2009. doi: 10.3748/wjg.15.2561
Human herpesvirus 6 infections after liver transplantation
Rima Camille Abdel Massih, Raymund R Razonable
Rima Camille Abdel Massih, Raymund R Razonable, Division of Infectious Diseases, Department of Medicine, and the William J von Liebig Transplant Center, College of Medicine, Mayo Clinic, Rochester, Minnesota 55905, United States
Author contributions: Abdel Massih RC and Razonable RR contributed to the conception, design, acquisition of data, drafting of the manuscript, and review of the final version of this paper.
Correspondence to: Raymund R Razonable, MD, Division of Infectious Diseases, Department of Medicine, and the William J von Liebig Transplant Center, College of Medicine, Mayo Clinic, Rochester, Minnesota 55905, United States. razonable.raymund@mayo.edu
Telephone: +1-507-2843747
Fax: +1-507-2844957
Received: March 26, 2009
Revised: April 11, 2009
Accepted: April 18, 2009
Published online: June 7, 2009
Abstract

Human herpesvirus 6 (HHV-6) infections occur in > 95% of humans. Primary infection, which occurs in early childhood as an asymptomatic illness or manifested clinically as roseola infantum, leads to a state of subclinical viral persistence and latency. Reactivation of latent HHV-6 is common after liver transplantation, possibly induced and facilitated by allograft rejection and immunosuppressive therapy. Since the vast majority of humans harbor the virus in a latent state, HHV-6 infections after liver transplantation are believed to be mostly due to endogenous reactivation or superinfection (reactivation in the transplanted organ). In a minority of cases, however, primary HHV-6 infection may occur when an HHV-6 negative individual receives a liver allograft from an HHV-6 positive donor. The vast majority of documented HHV-6 infections after liver transplantation are asymptomatic. In a minority of cases, HHV-6 has been implicated as a cause of febrile illness with rash and myelosuppression, hepatitis, pneumonitis, and encephalitis after liver transplantation. In addition, HHV-6 has been associated with a variety of indirect effects such as allograft rejection, and increased predisposition and severity of other infections including cytomegalovirus (CMV), hepatitis C virus, and opportunistic fungi. Because of the uncommon nature of the clinical illnesses directly attributed to HHV-6, there is currently no recommended HHV-6-specific approach to prevention. However, ganciclovir and valganciclovir, which are primarily intended for the prevention of CMV disease, are also active against HHV-6 and may prevent its reactivation after transplantation. The treatment of established HHV-6 disease is usually with intravenous ganciclovir, cidofovir, or foscarnet, complemented by reduction in the degree of immunosuppression. This article reviews the current advances in the pathogenesis, clinical diagnosis, and therapeutic modalities against HHV6 in the setting of liver transplantation.

Keywords: Immunocompromised; Antivirals; Human herpesvirus 6; Liver transplantation; Opportunistic infections