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Infectious spleen and kidney necrosis virus promotes replication organelle formation and sphingolipid biosynthesis to facilitate viral replication
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DOI：10.1016/j.fsi.2026.111646.png)
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Abstract
En 中文
• ISKNV infection remodels host lipid metabolism, with significant upregulation of glycerophospholipids, glycerolipids, and sphingolipids. • ISKNV increases unsaturated fatty acid-containing lipid levels from early infection, promoting the formation of viral replication organelle. • ISKNV activates sphingolipid biosynthesis at late infection via Spt and CerS, leading to ceramide accumulation. • Pharmacological inhibition of Spt or CerS suppresses viral replication, identifying these host lipid pathways as potential therapeutic targets against ISKNV.
Keywords:
Infectious spleen and kidney necrosis virus (ISKNV)
Lipid metabolism
Unsaturated fatty acid
Vesicle
Sphingolipid
Viral replication
Journal
F
IF:
3.9
Papers:
367
Citations:
0