Association of Human Herpesvirus 6 Reactivation with Severe Cytomegalovirus‐Associated Disease in Orthotopic Liver Transplant Recipients

DesJardin, Jeffrey A.; Cho, Eunhui; Supran, Stacey; Gibbons, Laurie; Werner, Barbara G.; Snydman, David R.

doi:10.1086/323336

Cited by 69 publications

(47 citation statements)

References 12 publications

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“…As a result of several in vitro analyses, HHV-6 has been demonstrated to have immunomodulatory effects such as impaired T cell activation, decreased cytokine synthesis, and impaired dendritic cell functions. [37][38][39][40] Although several investigators have suggested that HHV-6 infection is positively associated with CMV disease 15,17,18 and fungal infection 7 in liver transplant recipients, a definitive association between HHV-6 infection and these opportunistic infections remains unclear. This study showed no association between HHV-6 reactivation and CMV antigenemia or fungal infection.…”

Section: Discussionmentioning

confidence: 99%

“…1,2 Many investigators have studied the clinical features of HHV-6 infection in liver transplant recipients, using viral isolation, [3][4][5][6][7][8][9] antigenemia assay, [10][11][12][13][14] serological analysis, 15,16 and molecular analysis such as real-time polymerase chain reaction (PCR). [17][18][19][20][21][22] Several clinical features, including fever, 5,6,8,10 encephalitis, 7,23 CMV disease, 15,17,18 fungal infection, 7 graft dysfunction, 10,11,22 and hepatitis C virus (HCV) recurrence 9,19 after transplantation, have been suggested as clinical manifestations due to HHV-6 infection. However, the precise clinical features of HHV-6 reactivation remain unknown because evaluating active HHV-6 infection in transplant recipients is difficult.…”

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confidence: 99%

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Human herpesvirus 6 infection in adult living related liver transplant recipients

et al. 2007

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To analyze human herpesvirus 6 (HHV-6) infection in adult living related liver transplantation, we performed a virological analysis, including viral isolation, serological assay, and real-time polymerase chain reaction, of serially collected blood samples from 67 recipients. In addition, cytokine levels were measured to determine their role in viral reactivation. HHV-6 was isolated from only 4 recipients (6.0%), and viral DNA was detected in 15 (22.4%) of the 67 recipients. A significant increase in HHV-6 immunoglobulin G antibody titers was observed in 19 (28.4%) of the 67 recipients. Finally, 26 recipients (38.8%) had HHV-6 reactivation 2-6 weeks after transplantation. HHV-6 associated clinical features were analyzed in the 17 recipients presenting with either viremia or DNAemia. Two recipients with viremia and 3 recipients with DNAemia had unexplained fever at the time of viral infection. An increase in aminotransferase levels was observed in 2 recipients with viremia and 3 recipients with DNAemia. Recipients with liver cirrhosis caused by hepatitis B virus or hepatitis C virus infection as the underlying disease were more likely to have HHV-6 infection (P ϭ 0.025). Mortality at the last follow-up in recipients with HHV-6 reactivation was significantly higher than in those without viral reactivation (P ϭ 0.0118). Plasma interleukin-6 levels were significantly higher in the recipients with HHV-6 viremia than in the recipients without viremia at 4 weeks post-transplant (P ϭ 0.0411). Moreover, tumor necrosis factor ␣ levels were also higher in recipients with HHV-6 viremia (P Ͻ 0.0001) or reactivation (P ϭ 0.0011) than in recipients without viremia or reactivation 4 weeks post-transplant.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Human herpesvirus 6 infection in adult living related liver transplant recipients

et al. 2007

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“…27 Consistent with the results from our group, several investigators have also reported that infection with HHV-6 (and the degree of HHV-6 replication) and HHV-7 are associated with increased predisposition to invasive and symptomatic CMV disease. [56][57][58] Hepatitis C virus interaction. A potential interaction between HHV-6 and HHV-7 with other viral pathogens such as hepatitis C virus (HCV) may also exist.…”

Section: Indirect Effectsmentioning

confidence: 99%

The impact of human herpesvirus-6 and -7 infection on the outcome of liver transplantation

Razonable

Payá

2002

Liver Transplantation

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Human herpesvirus (HHV)-6 and -7 are novel members of the ␤-herpesvirus family that maintain latency in the human host after primary infection. Reactivation from latency and/or increased degree of viral replication occurs during periods of immune dysfunction. The clinical effect of HHV-6 and HHV-7 reactivation in recipients of liver transplants is now being recognized. Clinical illnesses such as fever, rash, pneumonitis, encephalitis, hepatitis, and myelosuppression have been described in a number of anecdotal reports. Moreover, a growing body of evidence suggests that the more important effect of HHV-6 and HHV-7 reactivation on the outcomes of liver transplantation may be mediated indirectly by their interactions with the other ␤-herpesvirus-cytomegalovirus (CMV). Coinfection among these three ␤-herpesviruses in clinical syndromes that were classically ascribed to be solely caused by CMV has been shown and has raised substantial interest in the potential role of HHV-6 and HHV-7 as copathogens in the direct and indirect illnesses caused by CMV. This article reviews the current scientific data on the role and the magnitude of impact of HHV-6 and HHV-7 infection on the outcomes of liver transplantation. (Liver Transpl 2002;8:651-658.)

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“…Some of the effects attributed to HHV-6 may actually be confounded by the action of CMV itself: Several reports noted a higher rate of CMV infection in patients with HHV-6 replication (38,(88)(89)(90)(91)(92)(93)(94)(95)(96)(97). A higher mortality rate associated with higher incidence of viral and fungal infections was observed in patients with HHV-6 (85).…”

Section: Type Of Organ Transplantmentioning

confidence: 99%

The Impact of Infection on Chronic Allograft Dysfunction and Allograft Survival After Solid Organ Transplantation

Martín-Gandul

Mueller

Pascual

et al. 2015

American Journal of Transplantation

131

103

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Infectious diseases after solid organ transplantation (SOT) are a significant cause of morbidity and reduced allograft and patient survival; however, the influence of infection on the development of chronic allograft dysfunction has not been completely delineated. Some viral infections appear to affect allograft function by both inducing direct tissue damage and immunologically related injury, including acute rejection. In particular, this has been observed for cytomegalovirus (CMV) infection in all SOT recipients and for BK virus infection in kidney transplant recipients, for community-acquired respiratory viruses in lung transplant recipients, and for hepatitis C virus in liver transplant recipients. The impact of bacterial and fungal infections is less clear, but bacterial urinary tract infections and respiratory tract colonization by Pseudomonas aeruginosa and Aspergillus spp appear to be correlated with higher rates of chronic allograft dysfunction in kidney and lung transplant recipients, respectively. Evidence supports the beneficial effects of the use of antiviral prophylaxis for CMV in improving allograft function and survival in SOT recipients. Nevertheless, there is still a need for prospective interventional trials assessing the potential effects of preventive and therapeutic strategies against bacterial and fungal infection for reducing or delaying the development of chronic allograft dysfunction.

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Association of Human Herpesvirus 6 Reactivation with Severe Cytomegalovirus‐Associated Disease in Orthotopic Liver Transplant Recipients

Cited by 69 publications

References 12 publications

Human herpesvirus 6 infection in adult living related liver transplant recipients

Human herpesvirus 6 infection in adult living related liver transplant recipients

The impact of human herpesvirus-6 and -7 infection on the outcome of liver transplantation

The Impact of Infection on Chronic Allograft Dysfunction and Allograft Survival After Solid Organ Transplantation

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