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      Association of tumour necrosis factor alpha and interleukin 6 levels with cytomegalovirus DNA detection and disease after renal transplantation.

      Journal of Medical Virology
      Adult, Cohort Studies, Cytomegalovirus, isolation & purification, physiology, Cytomegalovirus Infections, blood, etiology, immunology, DNA, Viral, analysis, Herpesvirus 6, Human, Herpesvirus 7, Human, Humans, Interleukin-6, Kidney Transplantation, adverse effects, Statistics, Nonparametric, Tumor Necrosis Factor-alpha, metabolism, Viral Load, Virus Activation

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          Abstract

          Cytokines such as tumour necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) are thought to be important in the pathogenesis of post-transplant cytomegalovirus (CMV) disease. CMV infection increases the production of TNF-alpha and IL-6. Conversely, TNF-alpha switches on the replication of CMV. To study the association of these two cytokines with CMV activity and disease, TNF-alpha and IL-6 levels were assayed in plasma samples taken serially from three groups of renal transplant recipients. Group A (n = 12) had CMV disease and syndrome; Group B (n = 11) had detectable CMV DNA in plasma or peripheral blood leucocytes without disease, i.e., presumed asymptomatic CMV infection, and Group C (n = 11) had no detectable CMV DNA nor disease. The median peak TNF-alpha levels in patients with CMV disease (Group A) were significantly higher than that in Group B or Group C (P < 0.02) whereas the median peak IL-6 levels in group C patients were significantly lower than that in group A (P < 0.04) or group B (P < 0.03). A TNF-alpha level of above 100 pg/ml was significantly associated with CMV disease and high plasma CMV load (> 10,000 copies/ml). IL-6 levels above 15 pg/ml were significantly associated with CMV DNA detection, but not with CMV disease or elevated CMV load. High levels of TNF-alpha or IL-6 were not associated with CMV donor/recipient serostatus, HHV-6 or HHV-7 DNA detection, immunosuppressive regimen or rejection episodes. The role of TNF-alpha in the pathogenesis of CMV disease deserves further investigation. Copyright 2001 Wiley-Liss, Inc.

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