Although the Epstein-Barr virus (EBV) infection is usually asymptomatic, a primary encounter with the virus can cause mononucleosis. EBV infection is also strongly associated with lymphoma and epithelial cancers. The structure and infection mechanism of EBV have been well studied, but the EBV-encoded G protein-coupled receptor, BILF1, is not fully understood. Here, it was found that the EBV BILF1 was expressed early in the viral lytic cycle and its ectopic expression strikingly upregulated the ICAM-1 expression in Raji cells. The positive effect of BILF1 on the ICAM-1 promoter was observed and the BILF1 deficiency attenuated ICAM-1 promoter activity. Moreover, NF-κB binding sites were important for the regulation of ICAM-1 promoter by BILF1. Furthermore, BILF1 reduced the constitutive level of the IқB-a protein and increased the amount of nuclear NF-қB in Raji cells. In conclusion, this study determined that BILF1 upregulated ICAM-1 in a mechanism involving NF-қB.

尽管爱泼斯坦巴尔病毒（EBV）感染通常是无症状的，但初次接触该病毒会引起单核细胞增多症。EBV感染也与淋巴瘤和上皮癌密切相关。EBV的结构和感染机理已得到很好的研究，但是尚未完全了解EBV编码的G蛋白偶联受体BILF1。在这里，发现EBV BILF1在病毒裂解周期的早期表达，其异位表达显着上调了Raji细胞中的ICAM-1表达。观察到BILF1对ICAM-1启动子的积极作用，而BILF1缺乏则减弱了ICAM-1启动子的活性。此外，NF-κB结合位点对ICAM-1的调节很重要BILF1的启动子。此外，BILF1降低了Raji细胞中IқB-a蛋白的组成水平，并增加了核NF-қB的含量。总之，这项研究确定BILF1在涉及NF-қB的机制中上调了ICAM-1。