Multiomics profiling of plasma reveals lipid-immune dysregulation and exosome remodeling in Mpox and Mpox–HIV co-infection

We hypothesized that MPXV infection induces significant remodeling of the host plasma lipidome, which is associated with viral pathogenesis. Furthermore, we postulated that HIV co-infection modulates this lipid response, resulting in a distinct lipid profile that differs from either MPXV or HIV mono-infection, potentially explaining the metabolic underpinnings of more severe disease outcomes in people with HIV.This dataset contains plasma lipidomic profiles from four participant groups across two study cohorts: (1) MPXV–HIV-coinfected (MPLWH), (2) MPXV-monoinfected (MPLWOH), (3) HIV-monoinfected (PLWH), (4) Healthy controls. Data was acquired using a liquid chromatography-tandem mass spectrometry (LC-MS/MS) platform，Raw data were processed for peak picking, integration, isotopic correction, and lipid identification, resulting in a final data matrix of relative lipid abundance. 195 lipid species were significantly altered in the Mpox groups compared to healthy controls. Shared increases were observed in phosphatidylserine (PS), phosphatidylethanolamine (PE), bis(monoacylglycerol)phosphate (BMP), ceramide (Cer), and long-chain sphingomyelin (SM). Shared decreases were found in phosphatidylcholine (PC), lysophosphatidylcholine (LPC), and cholesteryl ester (CE). This dataset can be reused by the research community to serve as a key reference for lipidomics studies on MPXV or HIV infection. The level of lipids was expressed as umol/mL.