ArticleViruses2018
Upregulation of Glucose Uptake and Hexokinase Activity of Primary Human CD4+ T Cells in Response to Infection with HIV-1.
Article in Viruses, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 93 citations in OpenAlex.
- Giardiavirus rewires host translation and glycolytic metabolism to support its replication inVirulence · 2026Article
- CAR signaling instructs divergent metabolic reprogramming and functional fates in αβ and γδ T cells.Cellular & molecular immunology · 2026Article
- Review
- Inflammation and RONS Dysregulation by Redox Enzymes as Mechanistic Links in HIV-1-Cancer Comorbidity.Pathogens (Basel, Switzerland) · 2026Review
- Nicotinamide metabolism is essential for Hepatitis C Virus replication and the production of infectious Lipo-Viro-Particles.PLoS pathogens · 2026Article
- Japanese encephalitis virus orchestrates GLUT4-mediated glucose metabolism to potentiate viral replication via insulin receptor signaling.PLoS pathogens · 2026Article
- Single-cell capture of on-ART SIV transcription reveals TGF-β-mediated metabolic control of viral latency.JCI insight · 2026Article
- The human plasma amino acids balance favours HIV replication in primary CD4 T lymphocytes.bioRxiv : the preprint server for biology · 2026Article
- Article
- Ferroptosis of T cell in inflammation and tumour immunity.Clinical and translational medicine · 2025Review
- Metabolic regulation of the immune system in health and diseases: mechanisms and interventions.Signal transduction and targeted therapy · 2024Review
- Targeting mitochondrial quality control: new therapeutic strategies for major diseases.Military Medical Research · 2024Review
- Flux Balance Analysis Reveals Potential Anti-HIV-1 Metabolic Targets.Infectious diseases & immunity · 2024Article
- Examining Chronic Inflammation, Immune Metabolism, and T Cell Dysfunction in HIV Infection.Viruses · 2024Review
- Oxidative phosphorylation in HIV-1 infection: impacts on cellular metabolism and immune function.Frontiers in immunology · 2024Review
- Activation of the JNK/COX-2/HIF-1α axis promotes M1 macrophage via glycolytic shift in HIV-1 infection.Life science alliance · 2023Article
- Membrane transporters in cell physiology, cancer metabolism and drug response.Disease models & mechanisms · 2023Review
- HIV-1 transmission: modelling and direct visualization in the third dimension.Microscopy (Oxford, England) · 2023Review
- 2-Deoxy-D-glucose inhibits lymphocytic choriomeningitis virus propagation by targeting glycoprotein N-glycosylation.Virology journal · 2023Article
- Advances in Immunotherapeutic Approaches to Type 1 Diabetes.International journal of molecular sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
Abstract
Infection of primary CD4+ T cells with HIV-1 coincides with an increase in glycolysis. We investigated the expression of glucose transporters (GLUT) and glycolytic enzymes in human CD4+ T cells in response to infection with HIV-1. We demonstrate the co-expression of GLUT1, GLUT3, GLUT4, and GLUT6 in human CD4+ T cells after activation, and their concerted overexpression in HIV-1 infected cells. The investigation of glycolytic enzymes demonstrated activation-dependent expression of hexokinases HK1 and HK2 in human CD4+ T cells, and a highly significant increase in cellular hexokinase enzyme activity in response to infection with HIV-1. HIV-1 infected CD4+ T cells showed a marked increase in expression of HK1, as well as the functionally related voltage-dependent anion channel (VDAC) protein, but not HK2. The elevation of GLUT, HK1, and VDAC expression in HIV-1 infected cells mirrored replication kinetics and was dependent on virus replication, as evidenced by the use of reverse transcription inhibitors. Finally, we demonstrated that the upregulation of HK1 in HIV-1 infected CD4+ T cells is independent of the viral accessory proteins Vpu, Vif, Nef, and Vpr. Though these data are consistent with HIV-1 dependency on CD4+ T cell glucose metabolism, a cellular response mechanism to infection cannot be ruled out.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.