EB病毒编码的 EBNA1 在成簇重复序列处导致11号染色体脆弱位点断裂。爱泼斯坦·巴尔病毒（Epstein Barr virus），简称EB病毒，我们身边最常见的疱疹病毒之一，十个人中有九个人感染。长久潜伏。EB病毒有时可能引起淋巴瘤、鼻咽癌、胃癌等多种癌症。本文是病毒引起的癌症的基础医学研究论文。
(Translated by Baidu: )
This virus infects 90% of people worldwide and is suspected of various cancers. New research in Nature reveals how it causes cancer
EBNA1 encoded by EB virus causes fragmentation of fragile site on chromosome 11 at clustered repetitive sequences. Epstein Barr virus, also known as EB virus, is one of the most common herpes viruses around us, with nine out of ten people infected. Long term incubation. EB virus can sometimes cause various cancers such as lymphoma, nasopharyngeal carcinoma, and gastric cancer. This article is a fundamental medical research paper on cancer caused by viruses.
（百度翻訳： ）
このウイルスは世界中の90%の人に感染し、複数のがんの疑いがある。『ネイチャー』の新研究では、どのようにがんを発症しているのかが明らかになった
EBウイルスによって符号化されたEBNA 1は、クラスタ化された繰り返し配列において、11番染色体脆弱部位の破断を引き起こす。エプスタイン・バルウイルス（Epstein Barr virus）、略称EBウイルス、私たちの身の回りで最もよく見られるヘルペスウイルスの1つ、10人中9人が感染しています。長く潜伏する。EBウイルスはリンパ腫、鼻咽頭癌、胃癌など多くの癌を引き起こす可能性がある。本文はウイルスによる癌の基礎医学研究論文である。
2023/04/20
论文
论文标题：Chromosomal fragile site breakage by EBV-encoded EBNA1 at clustered repeats
作者：Li, Julia Su Zhou, Abbasi, Ammal, Kim, Dong Hyun, Lippman, Scott M., Alexandrov, Ludmil B., Cleveland, Don W.
期刊：Nature
发表时间：2023/04/12
数字识别码：10.1038/s41586-023-05923-x
摘要：Epstein–Barr virus (EBV) is an oncogenic herpesvirus associated with several cancers of lymphocytic and epithelial origin1,2,3. EBV encodes EBNA1, which binds to a cluster of 20 copies of an 18-base-pair palindromic sequence in the EBV genome4,5,6. EBNA1 also associates with host chromosomes at non-sequence-specific sites7, thereby enabling viral persistence. Here we show that the sequence-specific DNA-binding domain of EBNA1 binds to a cluster of tandemly repeated copies of an EBV-like, 18-base-pair imperfect palindromic sequence encompassing a region of about 21 kilobases at human chromosome 11q23. In situ visualization of the repetitive EBNA1-binding site reveals aberrant structures on mitotic chromosomes characteristic of inherently fragile DNA. We demonstrate that increasing levels of EBNA1 binding trigger dose-dependent breakage at 11q23, producing a fusogenic centromere-containing fragment and an acentric distal fragment, with both mis-segregated into micronuclei in the next cell cycles. In cells latently infected with EBV, elevating EBNA1 abundance by as little as twofold was sufficient to trigger breakage at 11q23. Examination of whole-genome sequencing of EBV-associated nasopharyngeal carcinomas revealed that structural variants are highly enriched on chromosome 11. Presence of EBV is also shown to be associated with an enrichment of chromosome 11 rearrangements across 2,439 tumours from 38 cancer types. Our results identify a previously unappreciated link between EBV and genomic instability, wherein EBNA1-induced breakage at 11q23 triggers acquisition of structural variations in chromosome 11.
