Herpesvirus Infections in Solid Organ Transplant Patients at High Risk of Primary Cytomegalovirus Disease

Razonable, Raymund R.; Brown, Robert A.; Humar, Atul; Covington, E. Eugene; Alecock, Emma; Payá, Carlos V.

doi:10.1086/466529

Cited by 105 publications

(76 citation statements)

References 46 publications

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“…Thus, it has been suggested that the syndrome of febrile illness with myelosuppression and rash after transplantation be termed as b-herpesvirus syndrome while the specific viral etiology is being investigated [48] Co-infections with HHV-6 and CMV have been demonstrated in these cases [47] . However, a recent large study of solid organ transplant recipients demonstrated that HHV-6 was not significantly associated with any clinical symptoms during CMV disease [41] .…”

Section: Clinical Syndromes Associated With Hhv-6 Infection After LIVmentioning

confidence: 97%

“…The direct clinical manifestations due to HHV-6 include a febrile illness with or without rash, myelosuppression, hepatitis, pneumonitis and neurological diseases [33,[36][37][38] . The indirect effects attributed to HHV-6 include an exacerbation of cytomegalovirus (CMV) disease, an increased severity of hepatitis C virus (HCV) recurrence, an increased risk of other opportunistic infections, allograft dysfunction, and acute cellular rejection (Table 1) [33,36,[39][40][41][42][43][44][45] . Direct HHV-6 effects Fever and rash: The most frequently reported clinical presentation of HHV-6 infection after liver transplantation is a febrile illness that can be associated with a rash [34,36,46] .…”

Section: Clinical Syndromes Associated With Hhv-6 Infection After LIVmentioning

confidence: 99%

“…Fever and rash [36] Increased incidence and severity of cytomegalovirus disease [31,40,41] Hepatitis [33,36,49] Earlier and more severe recurrence of hepatitis C virus [42] Myelosuppression [37] Higher incidence of fungal infections [44] Pneumonitis [37] Higher incidence of opportunistic Infection [36] Neurologic illness [38,44,51] Higher incidence of allograft rejection [33,36,45,53] …”

Section: Hhv-6 Indirect Effectsmentioning

confidence: 99%

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Human herpesvirus 6 infections after liver transplantation

Massih¹,

Razonable²

2009

WJG

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Section: Clinical Syndromes Associated With Hhv-6 Infection After LIVmentioning

confidence: 97%

Section: Clinical Syndromes Associated With Hhv-6 Infection After LIVmentioning

confidence: 99%

Section: Hhv-6 Indirect Effectsmentioning

confidence: 99%

See 1 more Smart Citation

Human herpesvirus 6 infections after liver transplantation

Massih¹,

Razonable²

2009

WJG

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“…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%

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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“…For all other herpesviruses, in-house real-time polymerase chain reaction assays based on the Lightcycler format were performed on stored whole blood samples using methods previously described. 17 The lower limit of detection for these assays was ϳ5 copies/mL of whole blood. CMV viral load testing was done in all patients while other herpesviruses were tested for in patients who provided consent for these specific tests.…”

Section: Laboratory Testingmentioning

confidence: 99%

An assessment of interactions between hepatitis C virus and herpesvirus reactivation in liver transplant recipients using molecular surveillance

et al. 2007

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Hepatitis C virus (HCV) has been proposed to have immunomodulatory effects in transplant recipients and may promote herpesvirus reactivation. To assess this, we compared the incidence of herpesvirus reactivation in HCV-positive and HCVnegative liver transplant recipients. Quantitative viral load testing was performed at regular intervals posttransplantation for cytomegalovirus (CMV), Epstein-Barr virus (EBV), human herpesviruses (HHV) 6, 7, and 8, and varicella zoster virus (VZV) in 177 liver transplant patients who were HCV-positive (n ϭ 60) or HCV-negative (n ϭ 117). The incidence of CMV disease, CMV viremia, and the peak CMV viral load was not significantly different in HCV-positive vs. HCV-negative patients. Similarly, no differences in HHV-6 or EBV reactivation were observed. HHV-8 or VZV viremia was not detected in any patient in the study. A lower incidence of HHV-7 infection occurred in HCV-positive patients vs. HCV-negative patients (47.6% vs. 72.7%; P ϭ 0.006). In conclusion, these results suggest that HCV infection does not appear to promote herpesvirus reactivation after liver transplantation. Liver Transpl 13:1422Transpl 13: -1427Transpl 13: , 2007. © 2007 AASLD.Received February 19, 2007; accepted June 3, 2007. Cirrhosis caused by hepatitis C virus (HCV) infection is the leading indication for liver transplantation 1,2 and HCV viremia persists in up to 95% of patients posttransplantation. 3 By 5 yr posttransplantation, HCVinduced hepatitis and cirrhosis occur in approximately 80% and 10% of patients, respectively. 4,5 Herpesvirus reactivation is common after liver transplantation. Cytomegalovirus (CMV) infection and disease is especially common in CMV donor seropositive/recipient seronegative transplant recipients. Other herpesviruses, including human herpesviruses (HHV)-6 and HHV-7, also commonly reactivate after transplantation and coinfections with these viruses may manifest as febrile syndromes. 6 The interaction between herpesviruses and HCV has been proposed to be clinically important in HCV-infected liver transplant recipients. 7-10 CMV in particular may have immunomodulatory effects, and lead to cytokine dysregulation, resulting in a number of indirect effects such as an increased risk of opportunistic infection, posttransplantation lymphoproliferative disease (PTLD), and acute and chronic graft injury. 11 CMV 7 and HHV-6 7,9 have also been associated with more severe forms of HCV recurrence. Although fewer data are available, other immunomodulatory effects have also been proposed for other ␤-herpesviruses, including It is less clear whether HCV can promote herpes viralAbbreviations: HCV, hepatitis C virus; CMV, cytomegalovirus; EBV, Epstein-Barr virus; HHV, human herpesvirus; VZV, varicella zoster virus; PTLD, posttransplantation lymphoproliferative disease.

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Herpesvirus Infections in Solid Organ Transplant Patients at High Risk of Primary Cytomegalovirus Disease

Cited by 105 publications

References 46 publications

Human herpesvirus 6 infections after liver transplantation

Human herpesvirus 6 infections after liver transplantation

Human herpesvirus 6 infection in adult living related liver transplant recipients

An assessment of interactions between hepatitis C virus and herpesvirus reactivation in liver transplant recipients using molecular surveillance

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