High Temperature Influences on Virus–Host Interaction in Plants: A Case Study of Sweet Potato Virus Disease and Host Lipid Metabolism

Viral infections and high temperatures often occur together in the field, both of which alter lipid metabolism in plants. However, how RNA viruses manage plant lipid metabolism at high temperatures is largely unexplored. In this study, sweet potato virus disease (SPVD; co‐infection with Sweet potato feathery mottle virus [SPFMV] and Sweet potato chlorotic stunt virus )‐triggered remodeling of host lipid metabolism was characterized under different temperature regimes, using a combination of lipidomics, gene expression analysis, gene silencing, and pharmacology. SPVD remodeled leaf lipid metabolism under regular temperature conditions by predominantly increasing phospholipids, including phosphatidic acid, phosphatidylcholine, phosphatidylethanolamine, and phosphatidylinositol, coupled with a significant elevation of gene expression involved in phospholipid synthesis. Notably, SPVD increased phospholipids and significantly decreased triacylglycerols (TGs) during hot summer, coupled with a substantial elevation of gene expression involved in TG breakdown and phospholipid synthesis. Several TGs negatively correlated with phospholipid molecular species. Both diphenylmethylphosphonate (DMP) application and IbSDP1 silencing promoted TG accumulation at high temperature, which significantly inhibited the accumulation of SPFMV genomic RNA in SPVD‐infected sweet potato. This study highlights that high‐temperature‐induced TG accumulation can be utilized by SPFMV for synthesizing membrane lipids required for viral replication. These findings provide novel insights into the mechanisms through which viruses exploit host resources under specific environmental conditions.