Detection and monitoring of human herpesvirus 7 in adult liver transplant patients: impact on clinical course and association with cytomegalovirus |
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Authors: | Thomasini R L Sampaio A M Bonon S H A Boin I F S Leonardi L S Leonardi M Costa S C B |
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Affiliation: | 1. Department of Cardiology, St Vincent''s Hospital, Sydney, Australia;2. Department of Microbiology, St Vincent''s Hospital, Sydney, Australia;3. Department of Cardiology, Royal Prince Alfred Hospital, Sydney, Australia;4. Departments of Infectious Diseases and Microbiology, Royal Prince Alfred Hospital, Sydney, Australia;5. Faculty of Medicine, University of Sydney, Sydney, Australia |
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Abstract: | We herein have described HCMV and HHV-7 detection during the follow-up of 29 adult liver recipients in our transplant unit. For basic immunosuppression, the patients received cyclosporine and symptomatic HCMV infection was treated with gancyclovir. The most prevalent etiology for liver transplantation was hepatitis C or alcohol abuse (45% of patients). The laboratory monitoring to 180 days after transplantation was performed by nested-polymerase chain reaction to HCMV or HHV-7. HCMV DNA was detected in 19/29 of patients (65.5%) and HHV-7 DNA, in 14/29 of patients (48.2%). The time-related appearance of HHV-7 and HCMV DNA differed significantly (P = .02); their detection was considered independent (P = .2). The results showed that few patients remained free of HHV-7 or HCMV after liver transplantation, indicating that most patients were actively infected with more then one virus sequentially and not concurrently. Graft dysfunction, fever, gastrointestinal system abnormalities, and interstitial pneumonitis dominated the clinical pictures. Thirteen of 29 patients (44.8%) developed symptomatic HCMV active infections. The relationship between the detection of HCMV DNA, and HCMV disease development was significant (P = .0004). In HCMV-free patients, no symptoms or significant laboratory findings were linked with HHV-7. However, HHV-7 was frequently detected sequentially after HCMV, and an interaction of HCMV and/or HHV-6 to increase their pathogenic effects could not be excluded. Further studies should be performed including HHV-6 to evaluate the relationship, among beta herpesviruses. |
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