<p>Decapod iridescent virus 1 (DIV1) has emerged as a severe pathogen in the <i>Macrobrachium rosenbergii</i> aquaculture, causing substantial losses. While host physiological status influences disease resistance, the molecular mechanisms governing the interplay between ovary development and antiviral immunity remain poorly understood. In this study, we challenged previtellogenic (F1) and vitellogenic (F2) females by feeding DIV1-infected bait. Kaplan–Meier analysis showed that the state-specific mortality in F2 remained consistently lower than that in F1, and the 24-day cumulative mortality in F2 (34.7%) was significantly lower than that in F1 (44.3%). Subsequent time-series hepatopancreatic transcriptome analyses identified 2511 DEGs, with the F2 group displaying more pronounced transcriptional reprogramming throughout the infection. First, both groups exhibited Warburg effect signatures, characterized by the upregulation of hexokinase-2-like and downregulation of phosphoenolpyruvate carboxykinase. However, the F2 group simultaneously activated more pronounced expression of genes related to oxidative phosphorylation and the TCA cycle. Then, the F2 group exhibited a distinct defensive strategy. Pathways related to protein processing in the endoplasmic reticulum, proteasome, and N-glycan biosynthesis were significantly activated. Additionally, three core genes critical for lysosomal function—legumain-like, cathepsin D, and sialin-like—were specifically and significantly upregulated in the F2 group. Furthermore, an opposed expression pattern was observed between two major immune effectors: hemocyanin consistently displayed significantly lower expression in the F2 group, whereas multiple lectins, especially C-type lectin, displayed significantly higher basal expression or specific upregulation in the F2 group. These findings characterize the specific metabolic and immune configurations associated with the enhanced resistance of vitellogenic prawns to DIV1 infection, refining our understanding of the cooperative balance between reproduction and immunity.</p>

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Vitellogenesis enhances resistance to Decapod iridescent virus 1 in Macrobrachium rosenbergii through metabolic synergy and immune reconfiguration

  • Xinting Guan,
  • Jie Yang,
  • Wentao Xu,
  • Dayan Hu,
  • Quanxin Gao,
  • Zhenglong Xia,
  • Jiongying Yu,
  • Shaokui Yi

摘要

Decapod iridescent virus 1 (DIV1) has emerged as a severe pathogen in the Macrobrachium rosenbergii aquaculture, causing substantial losses. While host physiological status influences disease resistance, the molecular mechanisms governing the interplay between ovary development and antiviral immunity remain poorly understood. In this study, we challenged previtellogenic (F1) and vitellogenic (F2) females by feeding DIV1-infected bait. Kaplan–Meier analysis showed that the state-specific mortality in F2 remained consistently lower than that in F1, and the 24-day cumulative mortality in F2 (34.7%) was significantly lower than that in F1 (44.3%). Subsequent time-series hepatopancreatic transcriptome analyses identified 2511 DEGs, with the F2 group displaying more pronounced transcriptional reprogramming throughout the infection. First, both groups exhibited Warburg effect signatures, characterized by the upregulation of hexokinase-2-like and downregulation of phosphoenolpyruvate carboxykinase. However, the F2 group simultaneously activated more pronounced expression of genes related to oxidative phosphorylation and the TCA cycle. Then, the F2 group exhibited a distinct defensive strategy. Pathways related to protein processing in the endoplasmic reticulum, proteasome, and N-glycan biosynthesis were significantly activated. Additionally, three core genes critical for lysosomal function—legumain-like, cathepsin D, and sialin-like—were specifically and significantly upregulated in the F2 group. Furthermore, an opposed expression pattern was observed between two major immune effectors: hemocyanin consistently displayed significantly lower expression in the F2 group, whereas multiple lectins, especially C-type lectin, displayed significantly higher basal expression or specific upregulation in the F2 group. These findings characterize the specific metabolic and immune configurations associated with the enhanced resistance of vitellogenic prawns to DIV1 infection, refining our understanding of the cooperative balance between reproduction and immunity.