High glucose transporter 1 (Glut1) surface expression is associated with increased glycolytic activity in activated CD4+ T cells. Phosphatidylinositide 3‐kinases (PI3K) activation measured by p‐Akt and OX40 is elevated in CD4+Glut1+ T cells from HIV+ subjects. TCR engagement of CD4+Glut1+ T cells from HIV+ subjects demonstrates hyperresponsive PI3K‐mammalian target of rapamycin signaling. High basal Glut1 and OX40 on CD4+ T cells from combination antiretroviral therapy (cART)‐treated HIV+ patients represent a sufficiently metabolically active state permissive for HIV infection in vitro without external stimuli. The majority of CD4+OX40+ T cells express Glut1, thus OX40 rather than Glut1 itself may facilitate HIV infection. Furthermore, infection of CD4+ T cells is limited by p110γ PI3K inhibition. Modulating glucose metabolism may limit cellular activation and prevent residual HIV replication in ‘virologically suppressed’ cART‐treated HIV+ persons.
Metabolically active CD4+ T cells expressing Glut1 and OX40 preferentially harbor HIV during in vitro infection
Clovis S Palmer,G. Duette,Marc C E Wagner,D. Henstridge,S. Saleh,C. Pereira,Jingling Zhou,D. Simar,S. Lewin,M. Ostrowski,J. McCune,S. Crowe
Published 2017 in FEBS Letters
ABSTRACT
PUBLICATION RECORD
- Publication year
2017
- Venue
FEBS Letters
- Publication date
2017-10-01
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
CITATION MAP
EXTRACTION MAP
CLAIMS
- No claims are published for this paper.
CONCEPTS
- No concepts are published for this paper.
REFERENCES
Showing 1-61 of 61 references · Page 1 of 1
CITED BY
Showing 1-66 of 66 citing papers · Page 1 of 1