In immunocompetent individuals, EBV establishes in B cells an asymptomatic lifelong latent infection controlled by the immune system. Chemokine receptors regulate immune system function. CCR1 and CCR2 share protein sequence similarity and exert responses to multiple chemokines. The role of these receptors in B cells is largely unknown. We show that the mRNA and functional protein expression of CCR1 and CCR2 is induced in ex vivo B cells upon EBV infection and in established lymphoblastoid cell lines (LCLs). The CCR1 and CCR2B ORF transcripts were determined in LCLs. In contrast, in both the EBV-negative and EBV-positive Burkitt lymphoma cell lines, neither the CCR1, CCR2A, and CCR2B ORF transcripts nor their corresponding proteins were detected. Our data suggest that CCR1/CCR2B could be involved in clearing EBV-infected latency III B cells in immunocompetent individuals via directing the migration of these cells and attracting the chemokines-expressing immune cells.

在具有免疫能力的个体中，EBV在B细胞中建立了由免疫系统控制的无症状终身潜伏感染。趋化因子受体调节免疫系统功能。CCR1和CCR2共享蛋白质序列相似性，并对多种趋化因子产生反应。这些受体在B细胞中的作用在很大程度上是未知的。我们显示，CCB1和CCR2的mRNA和功能蛋白表达在EBV感染后在离体B细胞和已建立的淋巴母细胞样细胞系（LCL）中被诱导。该CCR1和CCR2B ORF转录物中的LCL确定。相反，在EBV阴性和EBV阳性Burkitt淋巴瘤细胞系中，CCR1，CCR2A和CCR2B ORF成绩单或相应的蛋白质均未检测到。我们的数据表明，CCR1 / CCR2B可能通过指导这些细胞的迁移并吸引表达趋化因子的免疫细胞参与免疫能力强的个体中被EBV感染的潜伏期III B细胞的清除。