Aguila-Toral Angela Camille, Silvederio Gardel Xyza L, Logronio Dan Joseph, Bateman Kelly S, Stentiford Grant D, Amar Edgar C, Ravago-Gotanco Rachel
The Marine Science Institute, College of Science, University of the Philippines Diliman, Quezon City 1101, Philippines.
The Marine Science Institute, College of Science, University of the Philippines Diliman, Quezon City 1101, Philippines.
J Invertebr Pathol. 2025 Sep 4:108450. doi: 10.1016/j.jip.2025.108450.
White spot syndrome virus (WSSV), the causative agent of white spot disease, remains a serious threat to crustacean aquaculture. Infecting a wide range of crustaceans, host species exhibit varying susceptibility and mortality rates. Mud crabs, Scylla serrata, a high-value aquaculture commodity across the Indo-Pacific region, are known to be relatively resistant to WSSV. However, there is limited information on the progression of WSSV infection in the species which can provide insight into mechanisms of resistance. Employing a time course experimental challenge of S. serrata with WSSV, this study characterized viral load dynamics in juveniles over a period of 144 h post infection (hpi) in relation to (1) disease outcomes (survival or mortality); (2) distribution among tissue types (gills, gut, hepatopancreas, and hemolymph); and (3) variability between two different juvenile cohorts. Viral load progression suggests that WSSV resistance in mud crabs may be due to two distinct mechanisms. One mechanism involves the capability of S. serrata for viral clearance following active viral replication. Viral growth in S. serrata demonstrates three phases: early stage or onset characterized by minimal change in viral load (0 to 24-hpi), logarithmic stage of active replication with rapid increase in viral copy number (24 to 72-hpi), with the third phase (96-144 hpi), exhibiting differential patterns with infection outcome. Dead crabs exhibited a plateau phase where viral loads remained similar to peak levels, while crabs that were still alive beyond 96 hpi exhibited a resolution phase, characterized by reduction in viral load, returning to non-infected levels. Another apparent mechanism for WSSV resistance involved overall inhibition of replication, with recalcitrant individuals exhibiting markedly low viral loads at expected logarithmic infection phase timepoints (48-72 hpi). This study also revealed tissue tropism of WSSV in S. serrata. Gills appear to be the primary site of WSSV replication, exhibiting the highest viral load from the early to peak stages of infection compared to other tissue types such as the gut, hepatopancreas, and hemolymph. The establishment of viral load curves to track the progression of WSSV infection, and characterization of viral abundance across different tissues through the course of infection, represents novel information that has key implications on the role of S. serrata as carriers/vectors of WSSV. This may have practical implications for disease mitigation measures for aquaculture facilities, and development of new strategies to prevent and reduce pathogen infection in mud crab to support sustainable aquaculture production.
白斑综合征病毒（WSSV）是白斑病的病原体，仍然对甲壳类水产养殖构成严重威胁。该病毒感染范围广泛的甲壳类动物，宿主物种表现出不同的易感性和死亡率。锯缘青蟹（Scylla serrata）是印度 - 太平洋地区一种高价值的水产养殖品种，已知对WSSV具有相对抗性。然而，关于该物种中WSSV感染进程的信息有限，而这些信息有助于深入了解抗性机制。本研究通过对锯缘青蟹进行WSSV的时间进程实验性攻毒，对感染后144小时内幼蟹的病毒载量动态进行了表征，涉及以下方面：（1）疾病结果（存活或死亡）；（2）在不同组织类型（鳃、肠道、肝胰腺和血淋巴）中的分布；（3）两个不同幼蟹群体之间的变异性。病毒载量的变化表明，锯缘青蟹对WSSV的抗性可能归因于两种不同的机制。一种机制涉及锯缘青蟹在病毒活跃复制后清除病毒的能力。锯缘青蟹体内的病毒生长呈现三个阶段：早期或发病阶段，病毒载量变化极小（0至24小时感染后）；活跃复制的对数期，病毒拷贝数迅速增加（24至72小时感染后）；而第三阶段（96 - 144小时感染后），根据感染结果呈现不同模式。死亡的螃蟹呈现出一个平台期，病毒载量保持在与峰值水平相似的状态，而在96小时感染后仍存活的螃蟹则呈现出消退期，其特征是病毒载量降低，恢复到未感染水平。另一种明显的WSSV抗性机制涉及对复制的整体抑制，顽固个体在预期的对数感染阶段时间点（48 - 72小时感染后）表现出极低的病毒载量。本研究还揭示了WSSV在锯缘青蟹中的组织嗜性。鳃似乎是WSSV复制的主要部位，与肠道、肝胰腺和血淋巴等其他组织类型相比，在感染的早期到峰值阶段呈现出最高的病毒载量。建立病毒载量曲线以追踪WSSV感染进程，并在感染过程中表征不同组织中的病毒丰度，代表了新的信息，对锯缘青蟹作为WSSV携带者/传播媒介的作用具有关键意义。这可能对水产养殖设施的疾病缓解措施以及制定预防和减少锯缘青蟹病原体感染的新策略以支持可持续水产养殖生产具有实际意义。
