HHV-6 was demonstrated in liver tissue by immunohistochemistry. A significant association between HHV-6 infection and CMV infection after transplantation, CMV recipient and donor serostatus, rejection, or fever of unknown origin, could not be documented. Pathogenesis of liver-induced damage associated to HHV6 remains unclear; however in vitro studies demonstrate the potential hepatotoxicity effects of this virus. All 9 isolates were HHV-6 variant B. Among these 4 recipients, 2 particularly immunosuppressed patients developed symptomatic diseases and died a few months after transplantation, harboring disseminated KS and HHV-8 positive lymphoproliferation. The aim of this study was to investigate their long-term course (9-14 years).
Of the 7 patients who had serological evidence of active HHV-6 infections but no evidence of CMV infection, 4 (56%) had fever, 1 (14%) hepatitis, 1 (14%) lung dysfunction, and 3 (42%) neurological disorders. An increase in aminotransferase levels was observed in 2 recipients with viremia and 3 recipients with DNAemia. Of the 7 patients who had serological evidence of active HHV-6 infections but no evidence of CMV infection, 4 (56%) had fever, 1 (14%) hepatitis, 1 (14%) lung dysfunction, and 3 (42%) neurological disorders. 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. For example, if the current year is 2008 and a journal has a 5 year moving wall, articles from the year 2002 are available. These findings suggest that patients with HLA-DR 15 in liver donor biopsies develop more rejection after liver transplantation.
Univariate analysis revealed HHV-6 infection was associated with the development of opportunistic infection and CMV disease. These findings suggest that patients with HLA-DR 15 in liver donor biopsies develop more rejection after liver transplantation. A higher rate of allograft rejection was observed in the CIHHV-6 group compared with the group with low-level HHV-6 DNAemia (71.4% vs. This is the first case report of a germinal center B cell-originating lymphoma with HHV-8 infection. Individualized treatment strategies are necessary given the scant body of published literature with guidance based solely on case reports. Notably, transcription of the genes encoding the MHV68 viral cyclin D homolog (v-cyclin) and the homolog of the KSHV latency-associated nuclear antigen (LANA), both of which are conserved among characterized γ2-herpesviruses, could consistently be detected in the established B cell lines.
Herpesvirus genome was detected by nested PCR in cloacal swabs, liver, and cloacal tissue samples. We report a case of 24 years-old Turkish woman with visceral HHV-8-associated Kaposi’s sarcoma after orthotopic liver transplantation. The majority of HHV-6 encephalitis has been limited to post-transplant recipients (Singh and Paterson 2000). Fulminant hepatic necrosis rarely has been reported after primary infection with the betaherpesviruses, human herpesviruses 6 and 7 (HHV-6 and HHV-7), which do not routinely cause hepatitis. IB detected IgM antibody to the 101-kDa protein in 75% (9 of 12) of the recipients. Forty-eight (54.4%) of 88 patients had at least 1 positive HHV-6 PCR.
A favorable evolution of the clinical symptoms and a progressive hematochemical resolution were obtained. However, infection of laboratory strains of mice with the rodent virus murine gammaherpesvirus 68 (MHV68) has been useful in gaining insights into how gammaherpesviruses contribute to the genesis and progression of lymphoproliferative lesions. METHODS: Peripheral blood and liver tissue were collected from 25 living related liver transplant recipients at the time of transplantation. To assess the incidence and morbidity of viral infections in immunosuppressed children, the authors conducted six-month postoperative studies of 51 consecutive pediatric patients undergoing liver transplantation. Whether HHV-6 plays a role in the occurrence of cytomegalovirus (CMV) infection after transplantation was investigated. Postmortem examination identified a pale, enlarged liver, mildly increased fluid in the lungs, and red foci in the spleen.
Primary HHV-6 infection was confirmed by demonstrating the seroconversion of HHV-6 antibodies with an immunofluorescence assay, by the isolation of the virus, or both. In addition, cytokine levels were measured to determine their role in viral reactivation. Interaction between the two viruses at the time of primary HHV-7 infection is suggested by in vivo and in vitro studies. 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.