ArticleCell cycle (Georgetown, Tex.)2015
Role of hexokinase-1 in the survival of HIV-1-infected macrophages.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
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- Hexokinase 1 cellular localization regulates the metabolic fate of glucose.Molecular cell · 2022Article
- Modulation of Macrophage Immunometabolism: A New Approach to Fight Infections.Frontiers in immunology · 2022Review
- Transcriptome Analysis of Genes Responding to Infection of Leghorn Male Hepatocellular Cells With Fowl Adenovirus Serotype 4.Frontiers in veterinary science · 2022Article
- Immunometabolism and HIV-1 pathogenesis: food for thought.Nature reviews. Immunology · 2021Review
- HIV-Sheltering Platelets From Immunological Non-Responders Induce a Dysfunctional Glycolytic CD4Frontiers in immunology · 2021Article
- The Role of Metabolic Enzymes in the Regulation of Inflammation.Metabolites · 2020Review
- Host-Directed Therapy in Tuberculosis: Targeting Host Metabolism.Frontiers in immunology · 2020Review
- The inert meets the living: The expanding view of metabolic alterations during viral pathogenesis.PLoS pathogens · 2019Review
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- Epigenome-wide association study of asthma and wheeze characterizes loci withinAllergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2019Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Viruses have developed various strategies to protect infected cells from apoptosis. HIV-1 infected macrophages are long-lived and considered reservoirs for HIV-1. One significant deciding factor between cell survival and cell death is glucose metabolism. We hypothesized that HIV-1 protects infected macrophages from apoptosis in part by modulating the host glycolytic pathway specifically by regulating hexokinase-1 (HK-1) an enzyme that converts glucose to glucose-6-phosphate. Therefore, we analyzed the regulation of HK-1 in HIV-1 infected PBMCs, and in a chronically HIV-1 infected monocyte-like cell line, U1. Our results demonstrate that HIV-1 induces a robust increase in HK-1 expression. Surprisingly, hexokinase enzymatic activity was significantly inhibited in HIV-1 infected PBMCs and in PMA differentiated U1 cells. Interestingly, we observed increased levels of mitochondria-bound HK-1 in PMA induced U1 cells and in the HIV-1 accessory protein, viral protein R (Vpr) transduced U937 cell derived macrophages. Dissociation of HK-1 from mitochondria in U1 cells using a pharmacological agent, clotrimazole (CTZ) induced mitochondrial membrane depolarization and caspase-3/7 mediated apoptosis. Dissociation of HK-1 from mitochondria in Vpr transduced U937 also activated caspase-3/7 activity. These observations indicate that HK-1 plays a non-metabolic role in HIV-1 infected macrophages by binding to mitochondria thereby maintaining mitochondrial integrity. These results suggest that targeting the interaction of HK-1 with the mitochondria to induce apoptosis in persistently infected macrophages may prove beneficial in purging the macrophage HIV reservoir.
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