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首页> 外文期刊>Journal of Medical Virology >Structural variability of the carboxy-terminus of Epstein-Barr virus encoded latent membrane protein 1 gene in Hodgkin's lymphomas.
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Structural variability of the carboxy-terminus of Epstein-Barr virus encoded latent membrane protein 1 gene in Hodgkin's lymphomas.

机译：霍奇金淋巴瘤中爱泼斯坦-巴尔病毒编码的潜在膜蛋白1基​​因的羧基末端的结构变异性。

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Epstein-Barr virus (EBV) is implicated in the pathogenesis of several lymphoid and epithelial neoplasms. Latent membrane protein 1 (LMP1) is the major viral oncogene and it is controversial whether tumor LMP1 variants reflect their geographical predominance or are associated with enhanced oncogenic properties. This study aimed to analyze LMP1 molecular variability of 62 EBV+ Hodgkin's lymphomas and 22 non-neoplastic controls from Brazil and Argentina. EBV association was characterized by EBER-ISH, LMP1 immunohistochemistry and PCR assays for EBNA2 and 3C (typing), LMP1 30 bp deletion (del30) and number of 33 bp tandem repeats. LMP1 C-terminal sequencing was performed in 42 cases. EBV1 was the predominant strain in both geographical Hodgkin's lymphoma groups (average 82%). A higher frequency of del30 variant was observed in lymphomas (41/63) than in non-neoplastic controls (6/22) (OR 4.97, CI 95% 1.53-16.79; P = 0.005, chi(2) test). A large number (5-7) of 33 bp repeat units was characteristic of del30 LMP1 variants (P < 0.0001, Fisher's exact test). Sequence analysis showed a similar mutation spectrum to that described worldwide but none of the current classification schemes could be applied completely. A distinct structural pattern was observed in del30 variants, characterized by a large number of 33 bp repeat units and the presence of a 15 bp insertion encoding the JAK3 Box-1a motif (3/15 wt vs. 16/20 del30; P = 0.001, chi(2) test). The results suggest a pathogenic role for LMP1 del30 variants in Hodgkin's lymphoma from South America and point to particular virus-host molecular mechanisms, such as genomic instability in LMP1 carboxy-terminus, leading to enhanced production and selection of these deletion variants.
机译：爱泼斯坦-巴尔病毒（EBV）与几种淋巴样和上皮性肿瘤的发病机制有关。潜伏膜蛋白1（LMP1）是主要的病毒致癌基因，对于肿瘤LMP1变体是否反映其地理优势还是与致癌性相关，尚存在争议。这项研究旨在分析来自巴西和阿根廷的62例EBV +霍奇金淋巴瘤和22例非肿瘤性对照的LMP1分子变异性。 EBV关联通过EBER-ISH，LMP1免疫组织化学和EBNA2和3C PCR检测（分型），LMP1 30 bp缺失（del30）和33 bp串联重复数进行表征。 LMP1 C端测序进行了42例。在两个地理霍奇金淋巴瘤组中，EBV1都是主要菌株（平均82％）。在淋巴瘤（41/63）中观察到的del30变异发生率高于非肿瘤对照组（6/22）（OR 4.97，CI 95％1.53-16.79; P = 0.005，chi（2）测试）。大量（5-7）33 bp重复单元是del30 LMP1变异体的特征（P <0.0001，Fisher精确检验）。序列分析显示出与世界范围内描述的突变谱相似的突变谱，但是目前的分类方案均无法完全应用。在del30变体中观察到了独特的结构模式，其特征在于大量的33 bp重复单元和编码JAK3 Box-1a基序的15 bp插入的存在（3/15 wt vs. 16/20 del30; P = 0.001 ，chi（2）测试）。结果表明，LMP1 del30变异体在南美霍奇金淋巴瘤中具有致病作用，并指向特定的病毒宿主分子机制，例如LMP1羧基末端的基因组不稳定性，从而导致这些缺失变异体的产生和选择增强。

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