ArticleScientific reports2019
HIV infection and latency induce a unique metabolic signature in human macrophages.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 2 of them syntheses that pooled it.
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Who cites it
77 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Pooled it
- Meta-Analysis on Nicotine's Modulation of HIV-Associated Dementia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2022Pooled it
- Integrative Multi-Omics Reveals Serum Markers of Tuberculosis in Advanced HIV.Frontiers in immunology · 2021Trial
- Review
- Glutamine Metabolism in Health and Diseases.MedComm · 2026Review
- Review
- Metabolic reprogramming of CD4⁺ T cells by Zaprinast induces HIV-1 latency reversal ex vivo.Retrovirology · 2026Article
- Sirtuin2 blockade inhibits replication of human immunodeficiency virus-1 and Mycobacterium tuberculosis in macrophages and humanized mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- HIV inhibits Warburg metabolism in human macrophages infected with Mycobacterium tuberculosis.Scientific reports · 2026Article
- Glycolysis inhibition in tuberculosis-driven metabolic rewiring reduces HIV-1 spread in macrophages.Life science alliance · 2026Article
- Cannabis use by people with HIV is associated with an anti-inflammatory immunometabolic phenotype in monocyte-derived macrophages.Journal of neuroinflammation · 2026Article
- Review
- Diagnostic value of miR-155, miR-29a and lncRNAs (NEAT1, GAS5 and COX2) in HIV, tuberculosis, and HIV/TB co-infection.Scientific reports · 2026Article
- Metabolomics of HIV in the Modern cART Era.Advances in experimental medicine and biology · 2026Review
- Pioglitazone Modulates p65-Mediated Mitochondrial Bioenergetics: Implications for Acetaldehyde-Induced HIV Replication in Alveolar Macrophages.Biomolecules · 2025Article
- Restriction of mitochondrial oxidation of glutamine or fatty acids enhances intracellular growth ofVirulence · 2025Article
- Single-Cell Multi-Modal Differential Analysis of the Human Neo-Cortex in HIV Infection Reveals Similarities with Hallmarks of Alzheimer's Disease.Research square · 2025Article
- Cannabinoid Receptor Type 2 Agonist JWH-133 Stimulates Antiviral Factors and Decreases Proviral, Inflammatory, and Neurotoxic Proteins in HIV-Infected Macrophage Secretome.International journal of molecular sciences · 2025Article
- Article
- Immuno-cell metabolic changes in HIV-1 infection.Infectious diseases & immunity · 2025Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Currently, a major barrier to curing HIV infection is the generation of tissue-associated, non-replicating, long-lasting viral reservoirs that are refractory to therapy and can be reactivated upon anti-retroviral therapy interruption. One of these reservoirs are latently HIV-infected macrophages. Here, we show that HIV infection of macrophages results in survival of a small population of infected cells that are metabolically altered and characterized by mitochondrial fusion, lipid accumulation, and reduced mitochondrial ATP production. No changes in glycolysis were detected. Metabolic analysis indicated an essential role of succinate and other TCA metabolites in the tricarboxylic acid (TCA) cycle in mediating lipid accumulation and oxidative phosphorylation (OXPHOS) in the mitochondria. Furthermore, we show that while uninfected and HIV infected macrophages use fatty acids and glucose as primary sources of energy, surviving HIV infected macrophages also use glutamine/glutamate as a major energy source, and blocking these new sources of energy resulted in the killing of latent HIV infected macrophages. Together, our data provide a new understanding of the formation, properties, and potential novel ways to eliminate macrophage viral reservoirs.
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