Upregulation of Glucose Uptake and Hexokinase Activity of Primary Human CD4+ T Cells in Response to Infection with HIV-1.
Upregulation of Glucose Uptake and Hexokinase Activity of Primary Human CD4+ T Cells in Response to Infection with HIV-1.
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原代人 CD4+ T 细胞响应 HIV-1 感染的葡萄糖摄取和己糖激酶活性上调。
DOI:
10.3390/v10030114
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发表时间:
2018-03-07
期刊:
影响因子:
--
通讯作者:
Huthoff H
中科院分区:
文献类型:
--
作者:
Kavanagh Williamson M;Coombes N;Juszczak F;Athanasopoulos M;Khan MB;Eykyn TR;Srenathan U;Taams LS;Dias Zeidler J;Da Poian AT;Huthoff H
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.
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DOI:
10.1097/qad.0000000000001320
发表时间:
2017-01-14
期刊:
AIDS (London, England)
影响因子:
--
作者:
Butterfield TR;Hanna DB;Kaplan RC;Kizer JR;Durkin HG;Young MA;Nowicki MJ;Tien PC;Golub ET;Floris-Moore MA;Titanji K;Fischl MA;Heath SL;Martinson J;Crowe SM;Palmer CS;Landay AL;Anzinger JJ
通讯作者:
Anzinger JJ
影响因子:
30.5
作者:
Chang CH;Pearce EL
通讯作者:
Pearce EL
影响因子:
64.5
作者:
Chang CH;Curtis JD;Maggi LB Jr;Faubert B;Villarino AV;O'Sullivan D;Huang SC;van der Windt GJ;Blagih J;Qiu J;Weber JD;Pearce EJ;Jones RG;Pearce EL
通讯作者:
Pearce EL
影响因子:
4.8
作者:
Grolleau, A;Bowman, J;Beretta, L
通讯作者:
Beretta, L
影响因子:
5.3
作者:
Gross, DN;Farmer, SR;Pilch, PF
通讯作者:
Pilch, PF