Introduction: Epstein-Barr virus (EBV) infection is common all over the world. Primary EBV infection can lead to latent or chronic infection resulting in lymphoproliferative diseases.
The Aim: of this study was to evaluate the effectiveness of laboratory methods used to detect EBV and to monitor EBV infections in children with acute leukaemia.
Materials And Methods: we conducted the study on 30 children with acute leukaemia. For the present analysis we included 8 patients from whom samples were also taken three times. Studies were made on serum, blood and bone marrow. Specific IgM and IgG antibodies for viral capsid antigen (VCA), nuclear (EBN) and early antigen (EA) were tested by ELSA. The presence of DNA virus was estimated by nested PCR. The control group were 11 subjects, without chronic or neoplastic disease, undergoing routine laboratory tests in the Virology Department.
Results: on admission serologied tests indicated past EBV infection in 6 out of the 8 children. Primary infection was detected in 2 patients, in one of them on day 1 of the observation and on day 22 in the other. DNA EBV was found by nested PCR in only one of the 8 infected children.
Conclusion: 1. Results of serological investigations indicated the type of EBV infection in our patients. 2. Confirmation of EBV virus active replication by nased PCR was obtained in only 1 out of 8 patients. 3. In order to assess the effectiveness of serological and molecular methods in evaluation of EBV infection type in children with acute leukaemia, it is necessary to investigate a larger group of patients and taken at least three times.
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Microbiol Mol Biol Rev
January 2025
Department of Molecular Genetics & Microbiology, Center for Virology, Duke University, Durham, North Carolina, USA.
SUMMARYInfection has long been hypothesized as the cause of multiple sclerosis (MS), and recent evidence for Epstein-Barr virus (EBV) as the trigger of MS is clear and compelling. This clarity contrasts with yet uncertain viral mechanisms and their relation to MS neuroinflammation and demyelination. As long as this disparity persists, it will invigorate virologists, molecular biologists, immunologists, and clinicians to ascertain how EBV potentiates MS onset, and possibly the disease's chronic activity and progression.
View Article and Find Full Text PDFVirol J
January 2025
Department of Pharmacotherapy, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
Introduction: Organ transplant recipients face a substantial risk of developing posttransplant lymphoproliferative disorders (PTLD). In over 90% of cases with B-cell PTLD following solid organ transplantation, the Epstein-Barr virus (EBV) genome is promptly identified, usually within the initial year. A continuing discussion revolves around the efficacy of antiviral prophylaxis in mitigating the incidence of PTLD in solid organ transplant (SOT) patients.
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January 2025
Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China.
Background: Primary pulmonary lymphoepithelial carcinoma (pLEC) is a subtype of non-small cell lung cancer (NSCLC) characterized by Epstein-Barr virus (EBV) infection. However, the molecular pathogenesis of pLEC remains poorly understood.
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Endocr Metab Immune Disord Drug Targets
December 2024
Institute of Neurobiology, Bulgarian Academy of Sciences, Acad. G. Bonchev St., Block 23, Sofia1113, Bulgaria.
Multiple Sclerosis (MS), a debilitating inflammatory disorder of the central nervous system characterized by demyelination, is significantly influenced by polygenic variations. Although the precise cause of MS remains unclear, it is believed to arise from a complex interplay of genetic and environmental factors. Recent investigations have focused on the polygenic nature of genetic alterations linked to MS risk.
View Article and Find Full Text PDFTurk J Pediatr
November 2024
Division of Pediatric Immunology, Department of Pediatrics, Hacettepe University Faculty of Medicine, Ankara, Türkiye.
Background: Griscelli syndrome (GS) is a rare genetic disorder characterized by oculocutaneous albinism and variable immune dysfunction. Among three distinct types of GS, occurring due to different genetic mutations; GS type 1 presents with neurological manifestations, hemophagocytic lymphohistiocytosis (HLH) generally develops in GS type 2, and GS type 3 primarily exhibits oculocutaneous albinism. HLH, a life-threatening condition with excessive immune activation, may occur secondary to various triggers, including infections, and develop in different tissues, as well as in the testis, similar to Erdheim-Chester disease.
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