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Metabolic pathways as regulators of HIV infection

Craveiro, Marco; Clerc, Isabelle; Sitbon, Marc; Taylor, Naomi

Current Opinion in HIV and AIDS: May 2013 - Volume 8 - Issue 3 - p 182–189
doi: 10.1097/COH.0b013e32835fc53e
STATE OF HIV CURE: Edited by Françoise Barré-Sinoussi and Michael M. Lederman

Purpose of review Activation of the immune system only occurs when stimulated cells generate sufficient energy to support their growth and proliferation. Moreover, efficient HIV-1 infection requires that CD4+ T cells meet the energy demands involved in completing the different steps of the virus life cycle. In this review, we highlight recent studies revealing the importance of nutrient fuels, nucleotide metabolism and the oxygen microenvironment in regulating HIV-1 infection, T-cell differentiation and the generation of HIV-1-specific immune responses.

Recent findings Glucose uptake via the Glut1 glucose transporter is required for efficient HIV-1 infection of CD4+ lymphocytes. Other nutrients can also be used as sources of energy and their utilization conditions the differentiation of CD4+ T cells to distinct effector fates. The conversion of ATP to adenosine inhibits HIV-specific effector cells and the hydrolysis of dNTPs by SAMHD1 restricts infection. Furthermore, oxygen concentration modulates metabolic status, thereby altering T-cell differentiation and potential to mediate a specific immune response.

Summary The availability and use of energy resources in fluctuating environments regulate T-cell function and susceptibility to HIV-1 infection. Identification of the targets coordinating the selected metabolic pathways will advance new strategic avenues for controlling HIV-1 disease progression.

Institut de Génétique Moléculaire de Montpellier, UMR 5535 CNRS, Université Montpellier 2, Université Montpellier 1, Montpellier, France

Correspondence to Marc Sitbon/Naomi Taylor, Institut de Génétique Moléculaire de Montpellier, 1919 Route de Mende, 34293 Montpellier, Cedex 5, France. Tel: +33 4 34 35 96 28; fax: +33 4 35 36 96 40; e-mail:,

© 2013 Lippincott Williams & Wilkins, Inc.