Integrated Lipidomic and Transcriptomic Analyses Reveal Stage-Specific Hepatic Lipid Remodeling during GCRV-II Infection in Grass Carp (Ctenopharyngodon idella).

Remodeling of host lipid metabolism by Wolbachia strain wAlbB is associated with lipid accumulation and cardiolipin dysregulation in the Aedes aegypti fat body

The intracellular symbiont Wolbachia , particularly the wAlbB strain, is a promising biocontrol agent against mosquito-borne diseases. Although Wolbachia infection is known to perturb host metabolism, the underlying mechanisms, especially those related to lipid metabolism, remain poorly understood. We performed an integrated multi-level analysis of the Aedes aegypti fat body in uninfected and wAlbB-infected mosquitoes, combining histology, biochemistry, untargeted liquid chromatography–mass spectrometry (LC–MS) lipidomics, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways enrichment analysis, reverse transcription quantitative PCR of key metabolic genes, and quantification of acetyl-coenzyme A (acetyl-CoA) and reduced nicotinamide adenine dinucleotide (NADH) levels. wAlbB infection increased fat body wet weight and thickness, accompanied by accumulation of triglyceride and of lipid droplets. Lipidomic analysis further revealed extensive lipidome remodeling, with elevated free fatty acid, diglyceride, and triglyceride, but broad depletion of glycerophospholipids, particularly cardiolipin . These changes were supported by transcriptional alterations: upregulation of fatty acid synthase 1 and glycerol-3-phosphate acyltransferase 1, and downregulation of adipose triglyceride lipase and carnitine palmitoyltransferase 1. Cardiolipin depletion correlated with downregulation of genes involved in its synthesis and remodeling, including phosphatidylglycerophosphate synthase and calcium-independent phospholipase A2γ. These lipid changes were also associated with accumulation of acetyl-CoA and NADH. Our findings suggest that wAlbB infection is associated with extensive lipid metabolic remodeling in the Aedes aegypti fat body, characterized by accumulation of neutral lipids and cardiolipin depletion, accompanied by transcriptional remodeling of key metabolic enzymes. This study establishes the fat body as a primary tissue-level hub for Wolbachia -associated lipid remodeling and provides a foundational framework for future mechanistic investigations into host–symbiont metabolic interactions.

Identification and analysis of lncRNA50877, which is involved in KRT8-mediated mitochondrial homeostasis and GCRV replication in grass carp (Ctenopharyngodon idella).

It is demonstrated that lncRNA50877 disrupts mitochondrial homeostasis by negatively regulating KRT8 expression, thereby modulating ROS levels, apoptosis, and autophagy; promoting oxidative stress-induced cell injury; and providing favorable conditions for GCRV replication.

Infectious spleen and kidney necrosis virus promotes replication organelle formation and sphingolipid biosynthesis to facilitate viral replication.

Infectious spleen and kidney necrosis virus (ISKNV) is a highly pathogenic iridovirus that causes severe economic losses in aquaculture. Viruses usually remodel host lipid metabolism to facilitate their replication. However, whether ISKNV modulates host lipid metabolism to support its infection remains unknown. In this study, using lipidomics analysis, we found that ISKNV infection induced widespread upregulation of host lipid profiles, including glycerophospholipids, glycerolipids, and sphingolipids. Transcriptional analysis revealed coordinated regulation of key metabolic enzymes, collectively favoring lipid accumulation. Notably, ISKNV infection increased the levels and proportions of unsaturated fatty acid-containing lipids from the early stage (24 hours post-infection, hpi), promoting the formation of membrane vesicles that act as replication organelles. Accordingly, transmission electron microscopy revealed abundant vesicles containing virions in infected cells at the late stage (72 hpi). Furthermore, lipidomics analysis demonstrated that ISKNV activated sphingolipid biosynthesis at 72 hpi, leading to ceramide accumulation. Pharmacological inhibition of serine palmitoyltransferase (Spt) or ceramide synthase (CerS) significantly suppressed viral replication, underscoring the functional importance of sphingolipid pathway. Collectively, these findings demonstrate that ISKNV hijacks host lipid metabolism through two mechanisms: 1) increasing of unsaturated fatty acid-containing lipids to facilitate the formation of viral replication organelles, and 2) activating sphingolipid biosynthesis to promote ceramide accumulation. This study provides a mechanistic basis for ISKNV pathogenesis and identifies host lipid metabolic pathways as potential therapeutic targets against this aquaculture pathogen.

Hepatitis C Virus Remodels Lipid Droplets to Promote Mitochondrial Fatty Acid Accumulation and Metabolic Activation

Temporal transcriptomic and lipidomic analysis reveals multi-omics dynamic profiles of B. napus seed germination.

BACKGROUND Lipids represent the major storage reserve in Brassica napus seeds. During germination, lipid mobilization delivers indispensable energy to support seedling establishment, thereby profoundly influencing germination vigor and subsequent seedling growth capacity. Although lipid mobilization is fundamentally required for successful rapeseed germination, the temporal coordination between transcriptional reprogramming and lipid metabolic conversion remains largely elusive, and the underlying molecular regulatory network remains to be systematically deciphered. RESULTS We conducted an integrated transcriptomic and lipidomic analysis on dry B. napus seeds and germinating seeds at 6, 12, 24, and 48 h after imbibition. The results revealed distinct stage-specific characteristics of gene expression and lipid metabolism during germination. In the early imbibition stage, differentially expressed genes (DEGs) were primarily enriched in biological processes related to water transport, stress response, and signal transduction, whereas significant changes in lipid metabolism were observed to be relatively delayed. During the initiation of germination, triacylglycerols (TGs) underwent rapid degradation, accompanied by a significant up-regulation of genes involved in the β-oxidation and gluconeogenesis pathways. In the late germination stage, genes responsible for membrane lipid synthesis were sharply up-regulated, which induced extensive membrane lipid remodeling. CONCLUSION This work represents the first systematic integration of transcriptomic and lipidomic data focusing on dynamic changes during the germination stage in B. napus, systematically illustrating the global molecular and lipid metabolic features of rapeseed seeds across sequential imbibition stages. It further delineates stage-specific expression patterns of key functional genes and lipid metabolites throughout germination. Collectively, these results advance our comprehensive understanding of the regulatory networks controlling rapeseed seed germination, and offer reliable theoretical references and candidate gene resources for breeding high-yield and high-quality B. napus varieties.

Tissue-Specific Transcriptomic Insights into Myxozoan Infections: Immune and Stress Responses in the Kidney and Head Cartilage of Rainbow Trout

By damaging target tissues and compromising the host immune system, Myxobolus cerebralis and Tetracapsuloides bryosalmonae remain persistent threats to salmonids. RNA sequencing was used to assess transcriptome modulation in the kidney and head cartilage (HC) of rainbow trout during single and co-infections with these two myxozoan parasites. Fish were exposed to M. cerebralis (Mc) and T. bryosalmonae (Tb), and 30 days later, half of the fish from each group were subjected to sequential co-infections (Mc+ and Tb+). This assessment aimed to evaluate the combined effects of both pathogens. Transcriptomic analysis was conducted using kidney and HC tissues collected 60 days post-co-infection. The results showed that infection order altered host transcriptional profiles in a tissue-dependent manner. In the kidney, Tb fish showed pronounced transcriptional alterations linked to chronic inflammation, immune complex clearance, and IL-8-mediated responses. Tb+ fish exhibited broad immune activation in the kidney, suggesting dysregulated inflammatory responses likely associated with subsequent infection with M. cerebralis. In the kidney of Mc+ fish, the immune response was characterized by macrophage and IL signaling pathways. In HC, Mc fish activated Th17, IL-23, phagolysosome, and IL-6 cytokine pathways. In contrast, Mc+ fish showed increased pathogen processing and enhanced metabolic responses accompanied by suppression of cytokines and tissue repair processes. HC responses in Tb+ fish shifted toward IL-23, Th17-driven responses, alongside reduced developmental and extracellular matrix processes. The study establishes that host responses to myxozoan co-infection are shaped by tissue tropism and infection sequence, with distinct immune and tissue remodeling pathways activated in the target organs. These findings enhance the understanding of sequential T. bryosalmonae and M. cerebralis infections and provide a basis for identifying tissue-specific biomarkers and key immune targets. The findings may help identify methods for improved monitoring and management of myxozoan infections in salmonids.