Chevaliez Stéphane, Balanant Jean, Maillard Patrick, Lone Yu-Chun, Lemonnier Francois A, Delpeyroux Francis
Unité de Biologie des Virus Entériques, Institut Pasteur, Paris, France.
Virology. 2008 Nov 25;381(2):203-14. doi: 10.1016/j.virol.2008.08.006. Epub 2008 Sep 27.
Several echoviruses use decay accelerating factor (DAF) as a cell surface receptor. However, most of them require additional cell surface coreceptors. We investigated the respective roles of DAF and class I human leukocyte antigen (HLA) molecules in the early steps of the echovirus 11 (EV11) lifecycle in rhabdomyosarcoma (RD) cells. EV11 infection was inhibited at an early stage by anti-beta2-microglobulin (beta2m) and anti-HLA monoclonal antibodies and by a soluble monochain HLA class I molecule. Expression of class I HLA molecules restored the early steps of the EV11 lifecycle, but its expression was not sufficient for EV11 replication and particle production. Expression of HLA class I molecules was associated with leukocyte cell line permissiveness to EV11 infection. In conclusion, HLA class I molecules are involved in the early steps of EV11 infection of RD cells and appear to participate in a complex interplay of surface molecules acting as coreceptors, including DAF.
几种肠道病毒使用衰变加速因子(DAF)作为细胞表面受体。然而,它们中的大多数还需要其他细胞表面共受体。我们研究了DAF和I类人类白细胞抗原(HLA)分子在横纹肌肉瘤(RD)细胞中肠道病毒11(EV11)生命周期早期阶段的各自作用。抗β2微球蛋白(β2m)和抗HLA单克隆抗体以及可溶性单链I类HLA分子在早期阶段抑制了EV11感染。I类HLA分子的表达恢复了EV11生命周期的早期步骤,但其表达不足以支持EV11复制和病毒颗粒产生。I类HLA分子的表达与白细胞细胞系对EV11感染的易感性相关。总之,I类HLA分子参与了RD细胞EV11感染的早期步骤,并且似乎参与了作为共受体的表面分子的复杂相互作用,包括DAF。