Back

Disrupted α-ketoglutarate homeostasis trains monocyte-derived macrophages towards M2-like phenotype in long-term treated HIV-infection

Escos, A.; Ambikan, A.; Schuster, S.; Svensson-Akusjärvi, S.; Gelpi, M.; Mansouri, S.; Naval, P.; Junior, R. L.; Sood, V.; Knudsen, A. D.; Pathade, P. P.; Mikaeloff, F.; Hogh, J.; Lourda, M.; Vesterbacka, J.; Nowak, P.; Benfield, T.; Pawar, V.; Siegfried, W.; Muvva, J. R.; Vegvari, A.; Gupta, S.; Savai, R.; Poulsen, S. D.; Neogi, U.

2025-01-19 systems biology
10.1101/2025.01.15.633214 bioRxiv
Show abstract

Cells of the myeloid lineage, particularly monocytes and macrophages, are central to HIV pathogenesis, contributing to viral persistence and immune regulation during suppressive therapy. We hypothesized that metabolic reprogramming and altered chemokine signaling in people with HIV (PWH) on long-term ART impair monocyte trafficking and macrophage polarization. Using single-cell RNA sequencing, immunophenotyping, and metabolic modeling, we identified altered receptor expression and disrupted metabolic flux linked to reduced monocyte migration. Plasma secretome profiling revealed a nonclassical inflammatory microenvironment, while integrative multi-omics and single-cell proteomics of monocyte-derived macrophages (MDMs) demonstrated metabolic rewiring of the Glycolysis-TCA Anaplerosis Axis, orchestrated in part by elevated -ketoglutarate (AKG). Differentiation with PWH serum or AKG, skewed MDMs toward an M2-like phenotype, and enhanced HIV susceptibility. Together, these systems-level and mechanistic analyses reveal that metabolic training drives macrophage dysfunction in well-treated PWH, sustaining low-grade inflammation and highlighting potential therapeutic targets.

Matching journals

The top 9 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.