Acute hepatopancreatic necrosis disease (AHPND) is a serious bacterial disease caused by V. parahaemolyticus strains which contain a virulent plasmid that encodes a binary pore-forming Pir toxin. Typically, these AHPND-causing bacteria first colonize in the shrimp stomach and then later cross to the hepatopancreas. To do this, they must pass through structural barriers which include the pliant cuticular lining of the stomach lumen. A previous transcriptomic study of shrimp challenged with the virulent 5HP strain of V. parahaemolyticus found significant upregulation of a contig associated with the cuticular proteins LvDD9A and LvDD9B. Here, we confirmed that the mRNA levels of these two genes were significantly upregulated not only in 5HP-infected shrimp, but also in the stomach of shrimp challenged with the white spot syndrome virus (WSSV). Using dsRNA-mediated gene silencing, we found that AHPND-causing bacteria migrated to the hepatopancreas within 3 h of AHPND infection in LvDD9A/B-silenced shrimp. Shrimp shell hardness of LvDD9A/B-silenced shrimp was also significantly decreased. Conversely, we found that silencing of LvDD9A/B significantly inhibited both WSSV gene expression and genome replication. Taken together, our data suggests that LvDD9A and LvDD9B are involved in both AHPND and WSSV infection. However, in AHPND, these cuticular proteins help to prevent bacterial migration from the stomach to the hepatopancreas, whereas in WSSV infection, they facilitate viral gene expression and genome replication.

急性肝胰腺坏死病 (AHPND) 是一种由副溶血性弧菌引起的严重细菌性疾病，其中含有编码二元成孔 Pir 毒素的毒性质粒。通常，这些引起 AHPND 的细菌首先在虾胃中定殖，然后再进入肝胰腺。要做到这一点，它们必须穿过包括胃腔柔韧表皮衬里在内的结构性屏障。先前对副溶血性弧菌5HP 毒株攻击的虾的转录组学研究发现，与表皮蛋白Lv DD9A 和Lv相关的重叠群显着上调DD9B。在这里，我们证实这两个基因的 mRNA 水平不仅在感染 5HP 的虾中显着上调，而且在受到白斑综合征病毒 (WSSV) 攻击的虾的胃中也显着上调。使用 dsRNA 介导的基因沉默，我们发现导致 AHPND 的细菌在LvDD9A/B沉默的虾的 AHPND 感染后 3 小时内迁移到肝胰腺。LvDD9A/B沉默虾的虾壳硬度也显着降低。相反，我们发现LvDD9A/B的沉默显着抑制了 WSSV 基因表达和基因组复制。综合来看，我们的数据表明Lv DD9A 和LvDD9B 参与 AHPND 和 WSSV 感染。然而，在 AHPND 中，这些表皮蛋白有助于防止细菌从胃迁移到肝胰腺，而在 WSSV 感染中，它们促进病毒基因表达和基因组复制。