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Epstein-Barr virus (EBV) is a fascinating microorganism, as a "double-facetted" viral agent. After primary infection, it can persist throughout a person's lifetime in a latent form, from which it can reactivate following specific stimuli (i.e., immunodepression). Unlike other herpesviruses, EBV reactivates a countless number of times with such a high replication rate that it is unable to be controlled by conventional anti-herpesvirus drugs. Moreover, for various reasons, no vaccine is currently available in the market. This book presents a comprehensive overview of EBV, including information on its potential for oncogenic activity, its various isolates, and possible vaccine candidates.

Epstein-Barr virus diseases.

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Epstein-Barr virus (EBV) is a fascinating microorganism, as a "double-facetted" viral agent. After primary infection, it can persist throughout a person's lifetime in a latent form, from which it can reactivate following specific stimuli (i.e., immunodepression). Unlike other herpesviruses, EBV reactivates a countless number of times with such a high replication rate that it is unable to be controlled by conventional anti-herpesvirus drugs. Moreover, for various reasons, no vaccine is currently available in the market. This book presents a comprehensive overview of EBV, including information on its potential for oncogenic activity, its various isolates, and possible vaccine candidates.

Epstein-Barr virus diseases.

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Epstein-Barr virus diseases --- Epstein-Barr virus --- Epstein-Barr Virus Infections --- Herpesvirus 4, Human --- Lymphoproliferative Disorders

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Aims. To investigate the role of interleukins 6 and 10 in primary EBV infection, and their predictive role in the development of post-transplant lymphoproliferative disease (PTLD) in pediatric orthotopic liver transplantation (OLT).
Patients and methods. Among 45 children who underwent OLT between 1998 and 2001 at Saint-Luc University Clinics, 12 children with primary EBV infection post-OLT were included. Patients were divided into two groups according to the evolution of primary EBV infection : group I (primary EBV infection without PTLD, n=6), and group II (primary EBV infection with PTLD, n=6). Median patient age was 1.5 years (range: 0.4 – 5.6) at the time of OLT. All children were regularly followed for clinical, biochemical and virological assessement. IL-6 and human IL-10 were measured in plasma by using the “sandwich” enzyme-linked immunoadsorbent assay (ELISA).
Results. Mean delay or primary EBV infection following OLT was 5,2 ± 1,1 weeks in group I, and 4,7 ± 0,6 weeks in group II (NS). PTLD occurred at 17,4 ± 18,2 weeks after OLT. Primary EBV infection was asymptomatic in all children. In group II, five (83.3%) children developed PTLSD with fever, three (50.0%) with tonsillitis, and one (16.7%) with stridor. Regarding the immunological assessement, IL-6 and IL-10 were detected in all patients during primary EBV infection and were correlated with the evolution of the patient’s cellular immunity and the viral load, respectively. The IL-6 and IL-10 serum levels did not differ significantly between the two groups at different time points of follow-up. In addition, the IL-6 and IL-10 levels in group II increased at the time of primary EBV infection, fluctuated after this infection, reaching a peak at the time of PTLD.
Conclusions. The presence of Il-6 was not specific for primary EBV infection in pediatric OLT. The increase of IL-10 following primary EBV infection might predict the development of PTLD. Further prospective studies are required to explore the role of IL-10 in the pathogenesis of PTLD Objectifs. Cette étude a été réalisée afin d’étudier l’évolution des interleukines (IL) 6 et 10 dans la primo-infection à EBV chez l’enfant transplanté hépatique, ainsi que leur rôle prédictif dans le développement d’un syndrome lymphoproliphératif (PTLD) associé à l’EBV chez ses enfants.
Patients et méthodes. Parmi 45 enfants transplantés hépatiques de 1998 à 2001 à Saint-Luc, douze enfants avec primo-infection à EBV post-transplantation ont été inclus. Les patients ont été divisés en deux groupes en fonction de l’évolution après la primo-infection à EBV : groupe I (primo-infection à EBV sans développement d’un syndrome lymphoprolifératif, n=6), et groupe II (primo-infection à EBV avec développement d’un syndrome lymphoprolifératif, n=6). L’âge médian des receveurs est de 1,5 ans (range : 0,4 – 5,6) au moment de la transplantation. Tous les patients ont été suivis régulièrement pour examen clinique, biochimie et virologie. Le dosage d’IL-6 et d’IL-10 humaine a été réalisé en utilisant la technique d’ELISA « sandwich ».
Résultats. Le délai moyen de la primo-infection est de 5,2 ± 1,1 semaines pour le groupe I, et de 4,7 ± 0,6 semaines pour le groupe II après la greffe (NS). Le PTLD est survenu après un délai moyen de 17,4 ± 18,2 semaines post-transplantation. La primo-infection est asymptomatique chez tous les patients. Dans le groupe II, les PTLD se manifestent cliniquement par une fièvre inexpliquée chez cinq (83,3%), angine chez trois (50,0%), et stridor chez un (16,7%) patients. Concernant le suivi immunologique, l’IL-6 et l’IL-10 sériques sont détectables dans les deux groupes pendant la primo-infection, en relation avec l’évolution de l’immunité cellulaire et de la charge virale, respectivement. La différence de concentrations d’IL-6 et d’IL-10 entre les 2 groupes n’est pas statistiquement significative à différents moments du suivi. Dans le groupe II, la concentration d’IL-6 et d’IL-10 est élevée au moment de la primo-infection, fluctuante durant les semaines suivant la primo-infection, et atteint un pic au moment du PTLD.
Conclusions. L’élévation de l’IL-6 n’est pas spécifique de la primo-infection à EBV en transplantation hépatique. La réaugmentation de l’IL-10 après la primo-infection EBV pourrait prédire l’évolution vers le PTLD. Des études prospectives seront nécessaires pour mettre en évidence son rôle dans le développement d’un PTLD

Liver Transplantation --- Interleukin-10 --- Interleukin-6 --- Epstein-Barr Virus Infections --- Child

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Epstein-Barr virus (EBV) is a ubiquitous virus that infects 95% of adults worldwide; the vast majority of persons have asymptomatic or non-specific primary infection and no complications associated with EBV during their lifetime. Some persons, particularly those who are infected as adolescents or young adults, develop infectious mononucleosis. EBV infects resting B cells and infection in vitro results in transformation and continuous proliferation of the cells, whereas infection in vivo results in a latent infection in which proliferation of the cells is controlled by virus-specific T cells and NK cells. Certain persons have mutations in genes that result in impaired cellular immunity involving the function of cytotoxic T cells or NK cells that result in impaired responses and failure to control EBV. These persons are at risk for fulminant infectious mononucleosis, EBV-associated hemophagocytosis, EBV B or T cell lymphoma, or other opportunistic infections. These genes encode proteins that are important for a variety of NK and T cell activities: T cell interactions with B cells, NK and T cell activation, NK and T cell cytotoxicity, priming and expansion of virus-specific T cells, and control of T cell apoptosis. For most of these diseases, hematopoietic stem cell transplantation has been the only curative therapy. However, identification of certain immune deficiencies has led to new approaches to therapy such as drugs to inhibit overactive signaling pathways or supplemental magnesium for patients with mutations in a magnesium transporter. The study of these EBV-associated immune deficiencies identifies the importance of these proteins for the function of T and NK cells and may lead to novel approaches to therapy for EBV diseases.

Medicine --- Immunology --- Epstein-Barr virus --- immune deficiency --- lymphoproliferative disease --- hemophagocytic lymphohistiocytosis --- B-cell lymphoma