Integrated lipidomic and transcriptomic analyses reveal stage-specific hepatic lipid remodeling during GCRV-II infection in grass carp (Ctenopharyngodon idella).

Grass carp reovirus genotype II (GCRV-II) is still a major threat to grass carp aquaculture and causes huge economic losses. Viral replication relies on host metabolic resources and metabolic reprogramming is key to virus-host interactions. However, the dynamic hepatic lipid remodeling associated with GCRV-II infection remains poorly understood. Here, the effect of GCRV-II infection on damage condition of liver from grass carp was evaluated and integrated lipidomic and transcriptomic was analyzed. Obviously, GCRV-II infection caused evident hepatic injury, significantly increased viral load and promoted hepatic lipid droplet accumulation. Lipidomic profiling revealed clear stage-dependent remodeling, characterized by broad glycerophospholipid perturbation at the early stage of infection, a sphingolipid- and acylcarnitine-dominant response at the middle stage, and persistent sphingolipid dysregulation with depletion of mitochondria-associated lipids at the late stage of infection. Meanwhile, LPE (20:4), Cer (43:2), and MePC (36:7e) were identified as the potential lipid biomarker corresponding to above three infected stages, respectively. Transcriptomic analysis also showed progressive disruption of lipid metabolism-related pathways, particularly glycerophospholipid metabolism, arachidonic acid metabolism, and sphingolipid metabolism, while fatty acid degradation became more prominent at the middle and late stages. Integrated analysis further revealed sustained glycerophospholipid remodeling and stage-specific sphingolipid dysregulation. These findings reveal temporally coordinated hepatic lipid metabolic reprogramming during GCRV-II infection and provide a foundation for further studies on how host lipid metabolism contributes to viral replication and pathogenesis.