Department of Virology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Department of Virology, Nagoya University Graduate School of Medicine, Nagoya, Japan; Department of Virology and Parasitology, Fujita Health University School of Medicine, Toyoake, Japan.
Virology. 2019 May;531:114-125. doi: 10.1016/j.virol.2019.02.015. Epub 2019 Feb 23.
The Epstein-Barr virus (EBV) is a causative agent of infectious mononucleosis and several malignancies. Here, we focused on an EBV lytic protein, BOLF1, which is conserved throughout the herpesvirus family and is reported to be a virion tegument protein. We first constructed BOLF1-deficient viruses using the bacterial artificial chromosome (BAC) and CRISPR/Cas9 systems. Although the loss of BOLF1 had almost no effect on viral protein expression, DNA synthesis, or extracellular progeny release, EBV infectivity was significantly reduced. Further analysis showed that nuclear transportation of the incoming virus was decreased by the disruption of BOLF1. Our results indicate that BOLF1enhances the infectious potential of progeny virions, at least partly by increasing nuclear transportation of incoming nucleocapsids. We also found that BOLF1 interacted with BKRF4, and the BOLF1 and BKRF4 proteins were localized in the nucleus and perinuclear area, during the viral lytic cycle.
EB 病毒（EBV）是传染性单核细胞增多症和几种恶性肿瘤的致病因子。在这里，我们专注于 EBV 裂解蛋白 BOLF1，它在疱疹病毒家族中是保守的，据报道是病毒衣壳蛋白。我们首先使用细菌人工染色体（BAC）和 CRISPR/Cas9 系统构建了 BOLF1 缺失病毒。尽管 BOLF1 的缺失几乎对病毒蛋白表达、DNA 合成或细胞外子代释放没有影响，但 EBV 的感染力显著降低。进一步的分析表明，BOLF1 的破坏降低了进入病毒的核转运。我们的结果表明，BOLF1 通过增加入核衣壳的核转运，增强了子代病毒颗粒的感染力。我们还发现 BOLF1 与 BKRF4 相互作用，并且在病毒裂解周期中，BOLF1 和 BKRF4 蛋白定位于核内和核周区。
