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Viruses 2018, 10(3), 114; https://doi.org/10.3390/v10030114

Upregulation of Glucose Uptake and Hexokinase Activity of Primary Human CD4+ T Cells in Response to Infection with HIV-1

1
Department of Infectious Diseases, King’s College London, Guy’s Hospital, London SE1 9RT, UK
2
Institute of Infection & Global Health, University of Liverpool, 8 W Derby St., Liverpool L7 3EA, UK
3
Faculty of Medicine and Pharmacy, University of Mons, Place du Parc 20, 7000 Mons, Belgium
4
Division of Imaging Sciences and Biomedical Engineering, The Rayne Institute, St. Thomas’ Hospital, King’s College London, Westminster Bridge Road, London SE1 7EH, UK
5
Centre for Inflammation Biology and Cancer Immunology (CIBCI), School of Immunology & Microbial Sciences, Department of Inflammation Biology, King’s College London, London SE1 1UL, UK
6
Instituto de Bioquímica Médica Leopoldo de Meis, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-902, Brazil
*
Author to whom correspondence should be addressed.
Received: 17 January 2018 / Revised: 28 February 2018 / Accepted: 1 March 2018 / Published: 7 March 2018
(This article belongs to the Section Animal Viruses)
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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. View Full-Text
Keywords: HIV-1; glycolysis; GLUT1; GLUT3; GLUT4; GLUT6; hexokinase; HK1; T lymphocytes HIV-1; glycolysis; GLUT1; GLUT3; GLUT4; GLUT6; hexokinase; HK1; T lymphocytes
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Kavanagh Williamson, M.; Coombes, N.; Juszczak, F.; Athanasopoulos, M.; Khan, M.B.; Eykyn, T.R.; Srenathan, U.; Taams, L.S.; Dias Zeidler, J.; Da Poian, A.T.; Huthoff, H. Upregulation of Glucose Uptake and Hexokinase Activity of Primary Human CD4+ T Cells in Response to Infection with HIV-1. Viruses 2018, 10, 114.

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