Immunology Unit, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Barcelona, 08036 Barcelona, Spain.
Institut d'Investigacions Biomèdiques August Pi i Sunyer, 08036 Barcelona, Spain.
Viruses. 2020 Jul 28;12(8):813. doi: 10.3390/v12080813.
The genesis of gene families by the capture of host genes and their subsequent duplication is a crucial process in the evolution of large DNA viruses. CD48 is a cell surface molecule that interacts via its N-terminal immunoglobulin (Ig) domain with the cell surface receptor 2B4 (CD244), regulating leukocyte cytotoxicity. We previously reported the presence of five CD48 homologs (vCD48s) in two related cytomegaloviruses, and demonstrated that one of them, A43, binds 2B4 and acts as a soluble CD48 decoy receptor impairing NK cell function. Here, we have characterized the rest of these vCD48s. We show that they are highly glycosylated proteins that display remarkably distinct features: divergent biochemical properties, cellular locations, and temporal expression kinetics. In contrast to A43, none of them interacts with 2B4. Consistent with this, molecular modeling of the N-terminal Ig domains of these vCD48s evidences notable changes as compared to CD48, suggesting that they interact with alternative targets. Accordingly, we demonstrate that one of them, S30, tightly binds CD2, a crucial T- and NK-cell adhesion and costimulatory molecule. Thus, our findings show how a key host immune receptor gene captured by a virus can be subsequently remodeled to evolve new immunoevasins with altered binding properties.
基因家族通过捕获宿主基因及其随后的复制而产生,是大型 DNA 病毒进化过程中的一个关键过程。CD48 是一种细胞表面分子,通过其 N 端免疫球蛋白 (Ig) 结构域与细胞表面受体 2B4(CD244)相互作用,调节白细胞细胞毒性。我们之前报道了两种相关巨细胞病毒中存在五种 CD48 同源物(vCD48),并证明其中一种 A43 与 2B4 结合,作为一种可溶性 CD48 诱饵受体,损害 NK 细胞功能。在这里,我们对其余的这些 vCD48 进行了特征描述。我们表明它们是高度糖基化的蛋白质,具有显着不同的特征:生化性质、细胞位置和时空表达动力学的差异。与 A43 不同,它们都不与 2B4 相互作用。与此一致,对这些 vCD48 的 N 端 Ig 结构域进行分子建模表明与 CD48 相比有明显的变化,表明它们与替代靶标相互作用。因此,我们证明其中一种 S30 与 CD2 紧密结合,CD2 是一种关键的 T 细胞和 NK 细胞黏附和共刺激分子。因此,我们的研究结果表明,病毒捕获的关键宿主免疫受体基因如何随后被重塑,以进化出具有改变结合特性的新免疫逃逸物。