ArticleJCI insight2020
Genomic variations in EBNA3C of EBV associate with posttransplant lymphoproliferative disorder.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- EBV Genome Variations and Association With Diseases.Journal of medical virology · 2026Review
- Epidemiology of Epstein-Barr Virus Chronic High Viral Load in Kidney Transplant Recipients.Transplantation direct · 2024Article
- Post-Transplant Lymphoproliferative Disorders.Seminars in nephrology · 2024Review
- Important Considerations in the Diagnosis and Management of Post-transplant Lymphoproliferative Disorder.Current oncology reports · 2023Review
- Clinical analysis of malignant lymphoma secondary to transplantation: the notorious lymphoproliferative disease.American journal of translational research · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Epstein-Barr Virus (EBV) is a ubiquitous virus linked to a variety of lymphoid and epithelial malignancies. In solid organ and hematopoietic stem cell transplant recipients, EBV is causally associated with posttransplant lymphoproliferative disorder (PTLD), a group of heterogeneous lymphoid diseases. EBV+ B cell lymphomas that develop in the context of PTLD are generally attributed to the immunosuppression required to promote graft survival, but little is known regarding the role of EBV genome diversity in the development of malignancy. We deep-sequenced the EBV genome from the peripheral blood of 18 solid organ transplant recipients, including 6 PTLD patients. Sequences from 6 EBV+ spontaneous lymphoblastoid B cell lines (SLCL) were similarly analyzed. The EBV genome from PTLD patients had a significantly greater number of variations than EBV from transplant recipients without PTLD. Importantly, there were 15 nonsynonymous variations, including 8 in the latent cycle gene EBNA3C that were associated with the development of PTLD. One of the nonsynonymous variations in EBNA3C is located within a previously defined T cell epitope. These findings suggest that variations in the EBV genome can contribute to the pathogenesis of PTLD.
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Registered trials
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