Publications & Reports

Glucose metabolism in T cells and monocytes: New perspectives in HIV pathogenesis.

Palmer CS, Cherry CL, Sada-Ovalle I, Singh A, Crowe SM

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.

This research was funded by the Australian Centre for HIV and Hepatitis Virology Research (ACH2) and a 2010 developmental grant (CNIHR) from the University of Washington Center for AIDS Research (CFAR), an NIH funded program under award number AI027757 which is supported by the following NIH Institutes and Centers (NIAID, NCI, NIMH, NIDA, NICHD, NHLBI, NIA). C.S.P. is a recipient of the CNIHR and ACH2 grant. S.M.C. is a recipient of a National Health and Medical Research Council of Australia (NHMRC) Principal Research Fellowship. A.S. is a recipient of CNIHR grant and acknowledges Indian C.S. Palmer et al. / EBioMedicine 6 (2016) 31–41 39 Council of Medical Research (ICMR, ICM 0067) for funding. The funders had no role in paper design, data collection, data analysis, interpretation, writing of the paper. The authors gratefully acknowledge the contribution to this work of the Victorian Operational Infrastructure Support Program received by the Burnet Institute. C.S.P would like to thank Mr Wallace Wainhouse at www.nice-consultants.com for graphic consultations.

Publication

  • Journal: EBioMedicine
  • Published: 05/02/2016
  • Volume: 6
  • Pagination: 31-41

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