Feederle R, Bannert H, Lips H, Müller-Lantzsch N, Delecluse H-J
Department of Virus Associated Tumours, German Cancer Research Center, ATV-F100, Im Neuenheimer Feld 242, 69120 Heidelberg, Germany.
J Virol. 2009 May;83(10):4952-62. doi: 10.1128/JVI.00170-09. Epub 2009 Mar 4.
The Epstein-Barr virus (EBV) alkaline exonuclease BGLF5 has previously been recognized to contribute to immune evasion by downregulating production of HLA molecules during virus replication. We have constructed a BGLF5-null virus mutant to determine BGLF5's functions during EBV viral replication. Quantification of virus production in permissive 293 cells carrying a DeltaBGLF5 genome identified a 17- to 21-fold reduction relative to complemented or wild-type controls. Detailed monitoring of DeltaBGLF5 replication evidenced an impaired virus nucleocapsid maturation, a reduced primary egress and a 1.4-fold reduction in total viral DNA synthesis. DeltaBGLF5 single-unit-length viral genomes were not only less abundant but also migrated faster than expected in gel electrophoresis. We concluded that BGLF5 pertained both to the generation and to the processing of viral linear genomes. DeltaBGLF5 phenotypic traits were reminiscent of those previously identified in a mutant devoid of UL12, BGLF5's homolog in herpes simplex virus type 1, and indeed UL12 was found to partially complement the DeltaBGLF5 phenotype. However, BGLF5-specific functions could also be identified; the nuclear membrane of replicating cells displayed images of reduplication and complex folding that could be completely corrected by BGLF5 but not UL12. Similar nuclear abnormalities were previously observed in cells transfected with BFLF2 and BFRF1, two viral proteins crucial for EBV nuclear egress. Interestingly, DeltaBGLF5 cells produced more BFLF2 than wild-type or complemented counterparts. The present study provides an overview of BGLF5's functions that will guide future molecular studies. We anticipate that the 293/DeltaBGLF5 cell line will be instrumental in such developments.
此前已认识到,爱泼斯坦-巴尔病毒(EBV)碱性核酸外切酶BGLF5通过在病毒复制过程中下调HLA分子的产生来促进免疫逃逸。我们构建了一种缺失BGLF5的病毒突变体,以确定BGLF5在EBV病毒复制过程中的功能。对携带ΔBGLF5基因组的允许性293细胞中的病毒产生进行定量分析,结果表明,与互补或野生型对照相比,病毒产量降低了17至21倍。对ΔBGLF5复制的详细监测表明,病毒核衣壳成熟受损,初次出芽减少,总病毒DNA合成减少了1.4倍。ΔBGLF5单单位长度的病毒基因组不仅数量较少,而且在凝胶电泳中的迁移速度比预期的要快。我们得出结论,BGLF5与病毒线性基因组的产生和加工有关。ΔBGLF5的表型特征让人想起之前在一种缺乏UL12的突变体中所发现的特征,UL12是单纯疱疹病毒1型中BGLF5的同源物,实际上发现UL12可以部分互补ΔBGLF5的表型。然而,也可以确定BGLF5的特异性功能;复制细胞的核膜显示出复制和复杂折叠的图像,这些图像可以被BGLF5完全纠正,但不能被UL12纠正。之前在转染了BFLF2和BFRF1的细胞中也观察到了类似的核异常,这两种病毒蛋白对EBV核出芽至关重要。有趣的是,ΔBGLF5细胞产生的BFLF2比野生型或互补型细胞更多。本研究概述了BGLF5的功能,将为未来的分子研究提供指导。我们预计293/ΔBGLF5细胞系将有助于此类研究的开展。