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Abstract

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.

Item Type:	Article
Authors/Creators:	Palmer, CS and Duette, GA and Wagner, MCE and Henstridge, DC and Saleh, S and Pereira, C and Zhou, J and Simar, D and Lewin, SR and Ostrowski, M and McCune, JM and Crowe, SM
Keywords:	cancer, CD4 T cells, Glut1, HIV, immunometabolism, mTOR, PI3K, CD134 antigen, CD4 antigen, glucose transporter 1, mammalian target of rapamycin, phosphatidylinositol 3 kinase, protein kinase B, protein p110 gamma, unclassified drug
Journal or Publication Title:	FEBS Letters
Publisher:	Elsevier Science Bv
ISSN:	0014-5793
DOI / ID Number:	10.1002/1873-3468.12843
Copyright Information:	Copyright 2017 The Authors. Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) http://creativecommons.org/licenses/by/4.0/
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