White spot syndrome virus (WSSV) is highly virulent toward shrimp, and F1 ATP synthase β subunit (ATPsyn-β) has been suggested to be involved in WSSV infection. Therefore, in this study, interactions between Penaeus monodon ATPsyn-β (PmATPsyn-β) and WSSV structural proteins were characterized. Based on the results of yeast two-hybrid, co-immunoprecipitation, and protein pull-down assays, WSSV VP51B and VP150 were identified as being able to interact with PmATPsyn-β. Membrane topology assay results indicated that VP51B and VP150 are envelope proteins with large portions exposed outside the WSSV virion. Cellular localization assay results demonstrated that VP51B and VP150 co-localize with PmATPsyn-β on the membranes of transfected cells. Enzyme-linked immunosorbent assay (ELISA) and competitive ELISA results demonstrated that VP51B and VP150 bound to PmATPsyn-β in a dose-dependent manner, which could be competitively inhibited by the addition of WSSV virions. In vivo neutralization assay results further showed that both recombinant VP51B and VP150 could delay mortality in shrimp challenged with WSSV.

白斑综合征病毒 (WSSV) 对虾具有高毒性，并且已提出 F1 ATP 合酶 β 亚基 (ATPsyn-β) 与 WSSV 感染有关。因此，在本研究中，斑节对虾之间的相互作用对 ATPsyn-β (PmATPsyn-β) 和 WSSV 结构蛋白进行了表征。基于酵母双杂交、共免疫沉淀和蛋白质下拉试验的结果，WSSV VP51B 和 VP150 被确定为能够与 PmATPsyn-β 相互作用。膜拓扑分析结果表明，VP51B 和 VP150 是包膜蛋白，大部分暴露在 WSSV 病毒体之外。细胞定位分析结果表明，VP51B 和 VP150 与 PmATPsyn-β 在转染细胞的膜上共定位。酶联免疫吸附试验 (ELISA) 和竞争性 ELISA 结果表明，VP51B 和 VP150 以剂量依赖性方式与 PmATPsyn-β 结合，可以通过添加 WSSV 病毒粒子来竞争性抑制。体内 中和试验结果进一步表明，重组VP51B和VP150都可以延缓受到WSSV攻击的虾的死亡率。