Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Qingdao, China.
Laboratory for Marine Biology and Biotechnology, Qingdao Marine Science and Technology Center, Qingdao, China.
PLoS Pathog. 2024 May 13;20(5):e1012228. doi: 10.1371/journal.ppat.1012228. eCollection 2024 May.
The arthropod exoskeleton provides protection and support and is vital for survival and adaption. The integrity and mechanical properties of the exoskeleton are often impaired after pathogenic infection; however, the detailed mechanism by which infection affects the exoskeleton remains largely unknown. Here, we report that the damage to the shrimp exoskeleton is caused by modulation of host lipid profiles after infection with white spot syndrome virus (WSSV). WSSV infection disrupts the mechanical performance of the exoskeleton by inducing the expression of a chitinase (Chi2) in the sub-cuticle epidermis and decreasing the cuticle chitin content. The induction of Chi2 expression is mediated by a nuclear receptor that can be activated by certain enriched long-chain saturated fatty acids after infection. The damage to the exoskeleton, an aftereffect of the induction of host lipogenesis by WSSV, significantly impairs the motor ability of shrimp. Blocking the WSSV-caused lipogenesis restored the mechanical performance of the cuticle and improved the motor ability of infected shrimp. Therefore, this study reveals a mechanism by which WSSV infection modulates shrimp internal metabolism resulting in phenotypic impairment, and provides new insights into the interactions between the arthropod host and virus.
节肢动物的外骨骼提供保护和支撑，对生存和适应至关重要。外骨骼的完整性和机械性能在受到病原感染后经常受损；然而，感染如何影响外骨骼的详细机制在很大程度上仍然未知。在这里，我们报告说，白斑综合征病毒（WSSV）感染后，宿主脂质谱的调节导致虾外骨骼受损。WSSV 感染通过在表皮下组织中诱导几丁质酶（Chi2）的表达并降低甲壳质含量来破坏外骨骼的机械性能。Chi2 表达的诱导是由一种核受体介导的，该受体在感染后可以被某些富集的长链饱和脂肪酸激活。WSSV 诱导的脂生成引起的外骨骼损伤，显著损害了虾的运动能力。阻断 WSSV 引起的脂生成恢复了甲壳的机械性能，并提高了感染虾的运动能力。因此，本研究揭示了 WSSV 感染调节虾体内代谢导致表型损伤的机制，并为节肢动物宿主与病毒之间的相互作用提供了新的见解。
