Department of Infectious Diseases and Microbiology, Graduate School of Public Health, University of Pittsburgh, 435 Parran Hall, 130 DeSoto Street, Pittsburgh, Pennsylvania, USA.
Virology. 2010 Apr 25;400(1):53-67. doi: 10.1016/j.virol.2010.01.002. Epub 2010 Feb 11.
EBV-immortalized B-lymphoblastoid cell lines are used as models for cellular transformation and as antigen-presenting cells in immunological assays. LCLs vary in surface markers and other phenotypic properties, but it is not known how this heterogeneity relates to the EBV life cycle. To explore correlations, we examined 62 LCLs for cellular and viral phenotypes. LCLs generated from pediatric and adult donors could similarly be categorized as either low in EBV copy number or fluctuating within a high range. High-copy status accompanied higher lytic viral gene expression and lower latent gene expression. Inhibiting lytic EBV replication did not affect cellular phenotype or lytic switch protein expression, indicating that an LCL's lytic permissivity was a stable property. Among the cellular genes overexpressed in permissive LCLs were unfolded protein response genes and plasma cell markers. Among genes overexpressed in non-permissive LCLs were transcription factors involved in maintaining B cell lineage, in particular EBF1. This study suggests previously undetected mechanisms by which cellular pathways influence the lytic reactivation of EBV.
EBV 永生化 B 淋巴细胞系被用作细胞转化的模型，并作为免疫测定中的抗原呈递细胞。LCL 在表面标志物和其他表型特性上存在差异，但尚不清楚这种异质性与 EBV 生命周期有何关系。为了探讨相关性，我们检查了 62 个 LCL 的细胞和病毒表型。来自儿科和成年供体的 LCL 可以相似地分为 EBV 拷贝数低或在高范围内波动。高拷贝数伴随着更高的裂解病毒基因表达和更低的潜伏基因表达。抑制裂解 EBV 复制不会影响细胞表型或裂解开关蛋白表达，表明 LCL 的裂解许可性是一种稳定的特性。在许可性 LCL 中过度表达的细胞基因包括未折叠蛋白反应基因和浆细胞标记物。在非许可性 LCL 中过度表达的基因包括参与维持 B 细胞谱系的转录因子，特别是 EBF1。这项研究表明，细胞途径影响 EBV 裂解再激活的机制以前未被发现。
