Evidence map›Paper›PMID 27211546›Full record

ReviewEBioMedicine2016

Glucose Metabolism in T Cells and Monocytes: New Perspectives in HIV Pathogenesis.

Clovis S Palmer, Catherine L Cherry, Isabel Sada-Ovalle, Amit Singh, Suzanne M Crowe

Open access · goldAbstract readReview
In one paragraph

Review in EBioMedicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
9.5field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Host-derived stimuli alter intracellular calcium levels inApplied and environmental microbiology · 2026
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20 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 3 countries.

Clovis S PalmerCentre for Biomedical Research, Burnet Institute, Melbourne, Australia; Department of Infectious Diseases, Monash University, Melbourne, Australia. Electronic address: cpalmer@burnet.edu.au.
Catherine L CherryCentre for Biomedical Research, Burnet Institute, Melbourne, Australia; Department of Infectious Diseases, Monash University, Melbourne, Australia; Infectious Diseases Department, The Alfred Hospital, Melbourne, Australia; School of Physiology, University of the Witwatersrand, Johannesburg, South Africa.
Isabel Sada-OvalleInstituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico.
Amit SinghDepartment of Microbiology and Cell Biology, Centre for Infectious Disease and Research (CIDR), Indian Institute of Science, India.
Suzanne M CroweCentre for Biomedical Research, Burnet Institute, Melbourne, Australia; Department of Infectious Diseases, Monash University, Melbourne, Australia; Infectious Diseases Department, The Alfred Hospital, Melbourne, Australia.
Burnet Institute · AUInstituto Nacional de Enfermedades Respiratorias · MXThe Alfred Hospital · AUUniversity of the Witwatersrand · ZA

Funding

University of Washington/Fred Hutch Center for AIDS ResearchP30AI027757 · NIAID · UNIVERSITY OF WASHINGTON · PI Kenneth Sherr · 1988 to 2026
$104.9M
NIAID NIH HHS P30 AI027757
6 · The paper itself

Abstract

Activation of the immune system occurs in response to the recognition of foreign antigens and receipt of optimal stimulatory signals by immune cells, a process that requires energy. Energy is also needed to support cellular growth, differentiation, proliferation, and effector functions of immune cells. In HIV-infected individuals, persistent viral replication, together with inflammatory stimuli contributes to chronic immune activation and oxidative stress. These conditions remain even in subjects with sustained virologic suppression on antiretroviral therapy. Here we highlight recent studies demonstrating the importance of metabolic pathways, particularly those involving glucose metabolism, in differentiation and maintenance of the activation states of T cells and monocytes. We also discuss how changes in the metabolic status of these cells may contribute to ongoing immune activation and inflammation in HIV- infected persons and how this may contribute to disease progression, establishment and persistence of the HIV reservoir, and the development of co-morbidities. We provide evidence that other viruses such as Epstein-Barr and Flu virus also disrupt the metabolic machinery of their host cells. Finally, we discuss how redox signaling mediated by oxidative stress may regulate metabolic responses in T cells and monocytes during HIV infection.

Indexed as

Disease ProgressionEpstein-Barr Virus InfectionsGlucoseHIV InfectionsHumansInfluenza, HumanLymphocyte ActivationMetabolic Networks and PathwaysMonocytesOxidative StressT-LymphocytesGlucoseCardiovascular diseaseCD4 T cellsCD8 T cellsGlucose transporter 1 (Glut1)HIVHIV cureHIV reservoirImmune activationImmunometabolismInflammationMacrophageMetabolismMonocytesOxidative stressSNAEs

Identifiers

PMID27211546
PMCPMC4856752
OpenAlexW2275746341

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.