Srinivas S K, Sample J T, Sixbey J W
St. Jude Children's Research Hospital, and Department of Pathology, University of Tennessee College of Medicine, Memphis 38105-2729, USA.
J Infect Dis. 1998 Jun;177(6):1705-9. doi: 10.1086/517427.
Life-long viral persistence is a hallmark of human herpesvirus infection. In the Epstein-Barr virus (EBV)-positive Burkitt's lymphoma (BL) cell line, Mutu, spontaneous loss of all viral episomes accompanied productive viral DNA replication. The molecular configuration of intracellular EBV DNA evolved from monoclonal episomes in cells retaining the original tumor phenotype to predominantly replicating linear DNA and, subsequently, only integrated forms in BL cells that had acquired the lymphoblastoid cell phenotype. Transient appearance of deleted, rearranged WZhet EBV DNA capable of disrupting viral latency, along with the integration of viral DNA into human chromosomes, indicates a genetic instability in the host cell which, if duplicated in vivo, may affect configuration and persistence of the viral genome in expanding malignant cell clones.
终生病毒持续存在是人类疱疹病毒感染的一个标志。在爱泼斯坦-巴尔病毒（EBV）阳性的伯基特淋巴瘤（BL）细胞系Mutu中，所有病毒附加体的自发丢失伴随着活跃的病毒DNA复制。细胞内EBV DNA的分子构型从保留原始肿瘤表型的细胞中的单克隆附加体演变为主要复制的线性DNA，随后在获得淋巴母细胞样细胞表型的BL细胞中仅为整合形式。能够破坏病毒潜伏状态的缺失、重排的WZhet EBV DNA的短暂出现，以及病毒DNA整合到人类染色体中，表明宿主细胞存在遗传不稳定性，如果在体内发生这种情况，可能会影响病毒基因组在不断扩大的恶性细胞克隆中的构型和持续性。
