Multiomics profiling of plasma reveals lipid-immune dysregulation and exosome remodeling in Mpox and MpoxHIV coinfection
Monkeypox virus (MPXV) infection and HIV co-infection are associated with systemic immune-metabolic dysregulation, but the cellular consequences of circulating exosome-mediated signaling remain incompletely understood. In this study, plasma-derived exosomes were isolated from healthy controls and from participants with Mpox without HIV (MPLWOH), Mpox-HIV co-infection (MPLWH), or HIV infection without Mpox (PLWH). Pooled exosome preparations from each group were used to treat HepG2 hepatocyte-like cells and A549 alveolar epithelial cells, followed by bulk RNA sequencing to characterize recipient-cell transcriptional responses. HepG2 cells were used to model hepatic lipid handling and metabolic stress, whereas A549 cells were used as an epithelial model for inflammatory, barrier-related, and tissue-remodeling responses. These RNA-seq data were generated as part of a multi-omics study integrating plasma lipidomics, metabolomics, exosome proteomics, cytokine profiling, and exosome-treated cell transcriptomics to investigate host lipid-immune dysregulation in Mpox and Mpox-HIV co-infection. The dataset provides transcriptomic evidence that patient-derived exosomes induce cell type-specific lipid metabolic and inflammatory programs, supporting functional interpretation of systemic plasma multi-omics signatures.