TY - JOUR
T1 - Human herpesvirus 6 infections after liver transplantation
AU - Massih, Rima Camille Abdel
AU - Razonable, Raymund R.
N1 - Funding Information:
The field dependence of C near T is shown in Fig. 3 for sample 3. The behavior dCffers from that of conventional type II superconductors in that the anomaly is diminished with increasing field but neither the temperature of the maximum in C/T nor the temperature of the onset of superconductivity is substantially affected. These features, which may reflect the importance of fluctuation effects, are similar to those observed in a single crystal (2) that showed a much sharper transition. The solid curve in Fig. 3 represents data for Y5, which shows no observable anomaly or field dependence in this temperature region, and which are therefore assumed to * Supported by the Director, Office of Energy Research, Office of Basic Energy Sciences, Materials Sciences Division of the U.S. Department of Energy under Contract DE-AC03-76SF00098. Additional support for J. E. G. was provided by an EXXON Education Grant from the Research Corporation an~ the Associated Western Universities - Department of Energy Sabbatical Participant Program. Permanent address: Physics Department, Amherst College, Amherst, MA 01002, USA
PY - 2009/6/7
Y1 - 2009/6/7
N2 - 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.
AB - 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.
KW - Antivirals
KW - Human herpesvirus 6
KW - Immunocompromised
KW - Liver transplantation
KW - Opportunistic infections
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U2 - 10.3748/wjg.15.2561
DO - 10.3748/wjg.15.2561
M3 - Editorial
C2 - 19496184
AN - SCOPUS:67651148221
SN - 1007-9327
VL - 15
SP - 2561
EP - 2569
JO - World journal of gastroenterology
JF - World journal of gastroenterology
IS - 21
ER -