Hijacking the Supplies: Metabolism as a Novel Facet of Virus-Host Interaction

Mayer, Katharina A.; Stöckl, Johannes; Zlabinger, Gerhard J.; Gualdoni, Guido A.

doi:10.3389/fimmu.2019.01533

Cited by 148 publications

(165 citation statements)

References 113 publications

(163 reference statements)

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“…Viruses are a major contributor to the global burden of diseases because they cause acute and chronic infectious diseases [26,27]. Many studies have shown how viruses hijack cellular pathways and evade the host's innate immune response, starting from entry, until the virus exits from host cells by modulating host factors and signaling pathways [28,29]. Therefore, comprehensive knowledge of host-virus interactions is important in order to understand the viral life cycle and to develop specific therapeutic approaches for the treatment of viral infections.…”

Section: Host-virus Interactionsmentioning

confidence: 99%

The Multifarious Role of 14-3-3 Family of Proteins in Viral Replication

Nathan

Lal

2020

Viruses

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The 14-3-3 proteins are a family of ubiquitous and exclusively eukaryotic proteins with an astoundingly significant number of binding partners. Their binding alters the activity, stability, localization, and phosphorylation state of a target protein. The association of 14-3-3 proteins with the regulation of a wide range of general and specific signaling pathways suggests their crucial role in health and disease. Recent studies have linked 14-3-3 to several RNA and DNA viruses that may contribute to the pathogenesis and progression of infections. Therefore, comprehensive knowledge of host–virus interactions is vital for understanding the viral life cycle and developing effective therapeutic strategies. Moreover, pharmaceutical research is already moving towards targeting host proteins in the control of virus pathogenesis. As such, targeting the right host protein to interrupt host–virus interactions could be an effective therapeutic strategy. In this review, we generated a 14-3-3 protein interactions roadmap in viruses, using the freely available Virusmentha network, an online virus–virus or virus–host interaction tool. Furthermore, we summarize the role of the 14-3-3 family in RNA and DNA viruses. The participation of 14-3-3 in viral infections underlines its significance as a key regulator for the expression of host and viral proteins.

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Section: Host-virus Interactionsmentioning

confidence: 99%

The Multifarious Role of 14-3-3 Family of Proteins in Viral Replication

Nathan

Lal

2020

Viruses

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“…Thus, it is not surprising that viruses and infected cells have co-evolved to develop measures and countermeasures to promote or restrict virus replication, respectively. This battle results in a profound impact of virus infection on the host cell's metabolism [1][2][3]. Also, this dependence of viruses on cell metabolism provides new intervention opportunities for limiting virus replication.…”

Section: Introductionmentioning

confidence: 99%

Metabolic changes during respiratory syncytial virus infection of epithelial cells

et al. 2020

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Viral infections induce substantial metabolic changes in infected cells to optimize viral production while cells develop countermeasures to restrict that infection. Human respiratory syncytial virus (HRSV) is an infectious pathogen that causes severe lower respiratory tract infections (LRTI) in infants, the elderly, and immunocompromised adults for which no effective treatment or vaccine is currently available. In this study, variations in metabolite levels at different time points post-HRSV infection of epithelial cells were studied by untargeted metabolomics using liquid chromatography/mass spectrometry analysis of methanol cell extracts. Numerous metabolites were significantly upregulated after 18 hours post-infection, including nucleotides, amino acids, amino and nucleotide sugars, and metabolites of the central carbon pathway. In contrast, most lipid classes were downregulated. Additionally, increased levels of oxidized glutathione and polyamines were associated with oxidative stress in infected cells. These results show how HRSV infection influences cell metabolism to produce the energy and building blocks necessary for virus reproduction, suggesting potential therapeutic interventions against this virus.

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“…[2][3][4][5][6][7] Many extensive reviews detail viral reprogramming of host cell metabolism, and for brevity, we refer readers elsewhere. [8][9][10][11] A variety of viruses stimulate increased glycolysis to drive the production of energy-rich molecules, such as ATP, NADH, and NADPH. Glycolysis can also supply a carbon pool for the synthesis of nucleotides, lipids, and amino acids for macromolecule production.…”

mentioning

confidence: 99%

Fueling influenza and the immune response: Implications for metabolic reprogramming during influenza infection and immunometabolism

Bahadoran

Bezavada

Smallwood

2020

Immunological Reviews

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The metabolic impact of influenza A virus (IAV) infections on immune cells remains largely uncharacterized. However, much is known about the metabolism of IAV infection and immunometabolism. Thus, we will consider four main factors: the metabolic requirements of influenza virus, metabolic reprogramming of immune cells that are mobilized to fight IAV infection, the impact of systemic or local metabolism on the infection and immune response, and vice versa. We will also address the interplay of metabolism and cytokines with a focus on those relevant to IAV infections. Finally, we will limit information on immunometabolism to key cell types critical to fighting IAV infection. We will relate this information to the unique metabolic demands on immune cells and discuss how their translocation through nutrient diverse and changing environments may affect their functions in IAV infection. | ME TABOLIS M AND THE LUNG MICROENVIRONMENT | Steady-state metabolismUnder aerobic conditions, cells sustain themselves catabolically using glycolytic carbons to fuel the tricarboxylic acid (TCA) cycle. AbstractRecent studies support the notion that glycolysis and oxidative phosphorylation are rheostats in immune cells whose bioenergetics have functional outputs in terms of their biology. Specific intrinsic and extrinsic molecular factors function as molecular potentiometers to adjust and control glycolytic to respiratory power output. In many cases, these potentiometers are used by influenza viruses and immune cells to support pathogenesis and the host immune response, respectively. Influenza virus infects the respiratory tract, providing a specific environmental niche, while immune cells encounter variable nutrient concentrations as they migrate in response to infection. Immune cell subsets have distinct metabolic programs that adjust to meet energetic and biosynthetic requirements to support effector functions, differentiation, and longevity in their ever-changing microenvironments. This review details how influenza coopts the host cell for metabolic reprogramming and describes the overlap of these regulatory controls in immune cells whose function and fate are dictated by metabolism. These details are contextualized with emerging evidence of the consequences of influenzainduced changes in metabolic homeostasis on disease progression. K E Y W O R D Shost pathogen, immune response, Immunometabolism, Influenza, metabolism, viral infection, virus | 141 BAHADORAN et Al.

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Hijacking the Supplies: Metabolism as a Novel Facet of Virus-Host Interaction

Cited by 148 publications

References 113 publications

The Multifarious Role of 14-3-3 Family of Proteins in Viral Replication

The Multifarious Role of 14-3-3 Family of Proteins in Viral Replication

Metabolic changes during respiratory syncytial virus infection of epithelial cells

Fueling influenza and the immune response: Implications for metabolic reprogramming during influenza infection and immunometabolism

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