Chikungunya virus (CHIKV), a mosquito-borne alphavirus, causes significant global mor-bidity, including fever, rash, and persistent arthralgia. Utilizing untargeted lipidomics, we investi-gated how CHIKV infection alters host cell lipid metabolism in Vero cells. CHIKV infection induced marked catabolism of hexosylceramides, reducing their levels while increasing ceramide byprod-ucts. Functional studies revealed a reliance on fatty acid synthesis, ?-oxidation, and glycosphin-golipid biosynthesis. Notably, inhibition of uridine diphosphate glycosyltransferase 8 (UGT8), es-sential for galactosylceramide production, significantly impaired CHIKV replication and entry. CHIKV was also sensitive to evacetrapib, a cholesterol ester transfer protein (CETP) inhibitor, though the mechanism of inhibition appeared independent of CETP itself, suggesting an off-target effect. These findings highlight specific lipid pathways, particularly glycosphingolipid metabolism, as critical for CHIKV replication and further refine our understanding of how CHIKV exploits host lipid networks. This study provides new insights into CHIKV biology and suggests that targeted investigation of host lipid pathways may inform future therapeutic strategies.
[doi:10.25345/C5CN6ZB57]
[dataset license: CC0 1.0 Universal (CC0 1.0)]
Keywords: lipidomics ; hexosylceramide ; CHIKV ; chikungunya ; DatasetType:Metabolomics
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Principal Investigators: (in alphabetical order) |
Kelly M. Hines, University of Georgia, USA Melinda A. Brindley, University of Georgia, USA |
| Submitting User: | kmhines5 |
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