Wang Mu, Sheng Xiu-Zhen, Xing Jing, Tang Xiao-Qian, Zhan Wen-Bin
Laboratory of Pathology and Immunology of Aquatic Animals, Ocean University of China, 5 Yushan Road, Qingdao 266003, PR China.
Dis Aquat Organ. 2011 Mar 16;94(1):9-16. doi: 10.3354/dao02311.
In vitro, lymphocystis disease virus (LCDV) infection of flounder gill (FG) cell cultures causes obvious cytopathic effect (CPE). We describe attempts to isolate and characterize the LCDV-binding molecule(s) on the plasma membrane of FG cells that were responsible for virus entry. The results showed that the co-immunoprecipitation assay detected a 27.8 kDa molecule from FG cells that bound to LCDV. In a blocking ELISA, pre-incubation of FG cell membrane proteins with the specific antiserum developed against the 27.8 kDa protein could block LCDV binding. Similarly, antiserum against 27.8 kDa protein could also inhibit LCDV infection of FG cells in vitro. Mass spectrometric analysis established that the 27.8 kDa protein and beta-actin had a strong association. These results strongly supported the possibility that the 27.8 kDa protein was the putative receptor specific for LCDV infection of FG cells.
在体外，淋巴囊肿病病毒（LCDV）感染牙鲆鳃（FG）细胞培养物会引起明显的细胞病变效应（CPE）。我们描述了分离和鉴定FG细胞膜上负责病毒进入的LCDV结合分子的尝试。结果表明，免疫共沉淀分析从FG细胞中检测到一个与LCDV结合的27.8 kDa分子。在阻断ELISA中，用针对27.8 kDa蛋白产生的特异性抗血清预孵育FG细胞膜蛋白可阻断LCDV结合。同样，针对27.8 kDa蛋白的抗血清也能在体外抑制FG细胞被LCDV感染。质谱分析确定27.8 kDa蛋白与β-肌动蛋白有很强的关联。这些结果有力地支持了27.8 kDa蛋白是FG细胞被LCDV感染的假定特异性受体的可能性。
