Chen Kuan-Yu, Hsu Tai-Ching, Huang Po-Yu, Kang Shih-Ting, Lo Chu-Fang, Huang Wei-Pang, Chen Li-Li
Institute of Marine Biology, National Taiwan Ocean University, Jhongjheng District, Keelung City 20224, Taiwan, ROC.
Fish Shellfish Immunol. 2009 Sep;27(3):460-5. doi: 10.1016/j.fsi.2009.06.018. Epub 2009 Jul 1.
White spot syndrome virus (WSSV) can cause the most serious viral disease of shrimp and has a wide host range among crustaceans. Although researches show a lot about its genome and structure, information concerning the mechanism of how WSSV infects' cells is lacking. In this study, some experiments were applied to confirm the biological meaning of the protein-protein interaction between WSSV envelope protein, VP53A, and Penaeus monodon chitin-binding protein (PmCBP). Immunofluorescent study indicated that PmCBP is located on the cell surface of host cells. PmCBP amounts of about 34kDa can be detected in both P. monodon and Litopenaeus vannamei tissues by Western blotting. In the in vivo neutralization experiment, both rVP53A and rPmCBP that were produced by Esherichia coli can promote resp. a 40% and 20% survival rate of the shrimp which were challenged by WSSV. Furthermore, a yeast-two-hybrid result revealed that PmCBP could interact with at least 11 WSSV envelope proteins. Those findings suggest that PmCBP may be involved in WSSV infection.
白斑综合征病毒（WSSV）可引发对虾最严重的病毒性疾病，并且在甲壳类动物中有广泛的宿主范围。尽管关于其基因组和结构已有很多研究，但关于WSSV如何感染细胞的机制信息却很缺乏。在本研究中，进行了一些实验以证实WSSV包膜蛋白VP53A与斑节对虾几丁质结合蛋白（PmCBP）之间蛋白质 - 蛋白质相互作用的生物学意义。免疫荧光研究表明，PmCBP位于宿主细胞的细胞表面。通过蛋白质印迹法在斑节对虾和凡纳滨对虾组织中均可检测到约34kDa的PmCBP量。在体内中和实验中，由大肠杆菌产生的rVP53A和rPmCBP均可分别提高受WSSV攻击的对虾40%和20%的存活率。此外，酵母双杂交结果显示PmCBP可与至少11种WSSV包膜蛋白相互作用。这些发现表明PmCBP可能参与WSSV感染。
