爱泼斯坦-巴尔病毒
淋巴增殖性病變
移植后淋巴增生性疾病
生物
免疫抑制
免疫学
背景(考古学)
基因组
恶性肿瘤
病毒
病毒学
淋巴瘤
基因
遗传学
古生物学
作者
Eden Maloney,Vincent Busque,Sin Ting Hui,Jiaying Toh,Marcelo Fernández-Viña,Sheri M. Krams,Carlos O. Esquivel,Olivia M. Martinez
出处
期刊:JCI insight
[American Society for Clinical Investigation]
日期:2020-03-26
卷期号:5 (6)
被引量:8
标识
DOI:10.1172/jci.insight.131644
摘要
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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