Metabolic pathways as regulators of HIV infection

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

doi:10.1097/coh.0b013e32835fc53e

Cited by 17 publications

(16 citation statements)

References 91 publications

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“…It is becoming increasingly evident that host cells employ metabolic regulatory mechanisms in order to restrict the life cycle of pathogens [1], [2], [3], [4]. The recent discovery of sterile alpha motif (SAM) domain and histidine-aspartic (HD) domain-containing protein 1 (SAMHD1) has contributed to our understanding of the metabolic regulation of deoxynucleoside triphosphates (dNTPs), the substrate for cellular DNA polymerases to synthesize and repair host DNA.…”

Section: Introductionmentioning

confidence: 99%

Host Factor SAMHD1 Restricts DNA Viruses in Non-Dividing Myeloid Cells

et al. 2013

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SAMHD1 is a newly identified anti-HIV host factor that has a dNTP triphosphohydrolase activity and depletes intracellular dNTP pools in non-dividing myeloid cells. Since DNA viruses utilize cellular dNTPs, we investigated whether SAMHD1 limits the replication of DNA viruses in non-dividing myeloid target cells. Indeed, two double stranded DNA viruses, vaccinia and herpes simplex virus type 1, are subject to SAMHD1 restriction in non-dividing target cells in a dNTP dependent manner. Using a thymidine kinase deficient strain of vaccinia virus, we demonstrate a greater restriction of viral replication in non-dividing cells expressing SAMHD1. Therefore, this study suggests that SAMHD1 is a potential innate anti-viral player that suppresses the replication of a wide range of DNA viruses, as well as retroviruses, which infect non-dividing myeloid cells.

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Section: Introductionmentioning

confidence: 99%

Host Factor SAMHD1 Restricts DNA Viruses in Non-Dividing Myeloid Cells

et al. 2013

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“…Observations that HIV infection is strongly associated with elevated plasma IL-7 (4) and that the virus overwhelmingly infects activated, but not resting, CD4 + T cells established the putative role of glycolysis in HIV pathogenesis (5–7). Loisel-Meyer et al (8) were the first to provide direct evidence for the role of glucose transporter 1 (Glut1) in regulating HIV entry into CD4 + T cells and thymocytes.…”

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confidence: 99%

Emerging Role and Characterization of Immunometabolism: Relevance to HIV Pathogenesis, Serious Non-AIDS Events, and a Cure

Palmer

Henstridge

et al. 2016

The Journal of Immunology

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Immune cells cycle between a resting and an activated state. Their metabolism is tightly linked to their activation status and, consequently, functions. Ag recognition induces T lymphocyte activation and proliferation and acquisition of effector functions that require and depend on cellular metabolic reprogramming. Likewise, recognition of pathogen-associated molecular patterns by monocytes and macrophages induces changes in cellular metabolism. As obligate intracellular parasites, viruses manipulate the metabolism of infected cells to meet their structural and functional requirements. For example, HIV-induced changes in immune cell metabolism and redox state are associated with CD4+ T cell depletion, immune activation, and inflammation. In this review, we highlight how HIV modifies immunometabolism with potential implications for cure research and pathogenesis of comorbidities observed in HIV-infected patients, including those with virologic suppression. In addition, we highlight recently described key methods that can be applied to study the metabolic dysregulation of immune cells in disease states.

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“…[206][207][208] It was observed that increased expression of the GLUT1 gene in interleukin-7-induced T-cells rendered CD4 T-cells and thymocytes susceptible to HIV-1 infection. 206,207 These reports suggest that the GLUT1-mediated metabolic pathway is the major regulator in HIV-infected cells. 207 Thus, GLUT1 could be a potential marker of a diseased heart and inflammation in HIV-infected subjects.…”

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confidence: 99%

Structure of, and functional insight into the GLUT family of membrane transporters

Long¹,

Cheeseman²

2015

CHC

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This review examines the development of structure and function of the human GLUT proteins, gene family hSLC2A. These proteins are essential for moving the key metabolites, glucose, galactose, and fructose in and out of cells, as well as a number of other important substrates. Despite over five decades of research, it is still not fully understood how they work at the molecular level, although the recent publication of a crystal structure of GLUT1 sug-

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Metabolic pathways as regulators of HIV infection

Abstract: 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.

Cited by 17 publications

References 91 publications

Host Factor SAMHD1 Restricts DNA Viruses in Non-Dividing Myeloid Cells

Host Factor SAMHD1 Restricts DNA Viruses in Non-Dividing Myeloid Cells

Emerging Role and Characterization of Immunometabolism: Relevance to HIV Pathogenesis, Serious Non-AIDS Events, and a Cure

Structure of, and functional insight into the GLUT family of membrane transporters

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