Effects of Interferons and Viruses on Metabolism

Fritsch, Stephanie Deborah; Weichhart, Thomas

doi:10.3389/fimmu.2016.00630

Cited by 105 publications

(117 citation statements)

References 151 publications

(194 reference statements)

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“…Interferons are well-known cytokines with a powerful capability of altering the cellular functions following viral infections. These alterations affect protein synthesis, composition of the membrane, cellular proliferation, and nutritional status [34]. Interferon stimulated genes (ISGs) are the effector components whose transcription could be induced by type I IFNs and IFNγ [114,115].…”

Section: Immunometabolites and Their Role In Influenza Infectionmentioning

confidence: 99%

“…Also, NO synthase-mediated generation of NO leads to the depletion of L-arginine, thereby reducing the level of polyamines. Thus, IFN-induced NOS2 represents antiviral activities, and this, in turn, may exhibit another mechanism through which IFNs hinder viral infections such as influenza [34]. Despite existing data regarding the antiviral activity of NO, many studies have considered NO as a double-edged sword with both pathogenic and viricidal effects.…”

Section: Ifns and Nitric Oxide Inductionmentioning

confidence: 99%

“…Since tryptophan is critical for T cell proliferation, depletion of this amino acid by IDO suppresses the immune system through the stimulation of T regulatory cells. NO, on the other hand, inhibits viral replication via changes in the structure of viral proteins [34]. In this review, we first discuss the metabolic abnormalities during influenza infection and then shed light on the role of immunometabolites that regulate cellular metabolism.…”

Section: Introductionmentioning

confidence: 99%

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Metabolic host response and therapeutic approaches to influenza infection

et al. 2020

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Based on available metabolomic studies, influenza infection affects a variety of cellular metabolic pathways to ensure an optimal environment for its replication and production of viral particles. Following infection, glucose uptake and aerobic glycolysis increase in infected cells continually, which results in higher glucose consumption. The pentose phosphate shunt, as another glucose-consuming pathway, is enhanced by influenza infection to help produce more nucleotides, especially ATP. Regarding lipid species, following infection, levels of triglycerides, phospholipids, and several lipid derivatives undergo perturbations, some of which are associated with inflammatory responses. Also, mitochondrial fatty acid βoxidation decreases significantly simultaneously with an increase in biosynthesis of fatty acids and membrane lipids. Moreover, essential amino acids are demonstrated to decline in infected tissues due to the production of large amounts of viral and cellular proteins. Immune responses against influenza infection, on the other hand, could significantly affect metabolic pathways. Mainly, interferon (IFN) production following viral infection affects cell function via alteration in amino acid synthesis, membrane composition, and lipid metabolism. Understanding metabolic alterations required for influenza virus replication has revealed novel therapeutic methods based on targeted inhibition of these cellular metabolic pathways.

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Section: Immunometabolites and Their Role In Influenza Infectionmentioning

confidence: 99%

Section: Ifns and Nitric Oxide Inductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Metabolic host response and therapeutic approaches to influenza infection

et al. 2020

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“…Finally, PDC express IFNAR, the membrane receptor for type I IFN (IFN-α or IFN-β) that consists of two subunits, IFNAR1 and IFNAR2. Engagement of this receptor by its ligand activates JAK1 (associated with IFNAR1) and tyrosine kinase 2 (associated with IFNAR2) that phosphorylate and activate STAT1 and STAT2, respectively ( Figure 1) 66, 67 .…”

Section: The Innate Immune Functions Of Plasmacytoid Dendritic Cellsmentioning

confidence: 99%

Recent insights into the implications of metabolism in plasmacytoid dendritic cell innate functions: Potential ways to control these functions

Saas¹,

Varin²,

Perruche³

et al. 2017

F1000Res

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There are more and more data concerning the role of cellular metabolism in innate immune cells, such as macrophages or conventional dendritic cells. However, few data are available currently concerning plasmacytoid dendritic cells (PDC), another type of innate immune cells. These cells are the main type I interferon (IFN) producing cells, but they also secrete other pro-inflammatory cytokines (e.g., tumor necrosis factor or interleukin [IL]-6) or immunomodulatory factors (e.g., IL-10 or transforming growth factor-β). Through these functions, PDC participate in antimicrobial responses or maintenance of immune tolerance, and have been implicated in the pathophysiology of several autoimmune diseases. Recent data support the idea that the glycolytic pathway (or glycolysis), as well as lipid metabolism (including both cholesterol and fatty acid metabolism) may impact some innate immune functions of PDC or may be involved in these functions after Toll-like receptor (TLR) 7/9 triggering. Some differences may be related to the origin of PDC (human versus mouse PDC or blood-sorted versus FLT3 ligand stimulated-bone marrow-sorted PDC). The kinetics of glycolysis may differ between human and murine PDC. In mouse PDC, metabolism changes promoted by TLR7/9 activation may depend on an autocrine/paracrine loop, implicating type I IFN and its receptor IFNAR, explaining a delayed glycolysis. Moreover, PDC functions can be modulated by the metabolism of cholesterol and fatty acids. This may occur via the production of lipid ligands that activate nuclear receptors (e.g., liver X receptor [LXR]) in PDC or through limiting intracellular cholesterol pool size (by statins or LXR agonists) in these cells. Finally, lipid-activated nuclear receptors ( i.e., LXR or peroxisome proliferator activated receptor) may also directly interact with pro-inflammatory transcription factors, such as NF-κB. Here, we discuss how glycolysis and lipid metabolism may modulate PDC functions and how this may be harnessed in pathological situations where PDC play a detrimental role.

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“…(2017), которые идентифицировали аллельные варианты генов HLA системы при элиминации вируса гепатита С [7]. В по-следующих работах исследовался уровень экспрес-сии генов интерферона-γ (IFN-γ), интерлейкина-1 (IL-1), фактора некроза опухоли-α (TNF-α), интер-лейкина-10 (IL-10) и была определена их роль как предикторов персистенции или элиминации вируса гепатита С [9].…”

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