Viral hijacking of cellular metabolism

Thaker, Shivani K.; Ch’ng, James; Christofk, Heather R.

doi:10.1186/s12915-019-0678-9

Cited by 392 publications

(441 citation statements)

References 153 publications

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“…Our understanding of the host immune response to SARS-CoV-2 infection is limited, making it difficult to design novel therapeutics. Viral infection usually causes massive alterations in the host transcriptome, leading to aberrant host cell metabolism and modulated immune response which is ideal for viral replication [12,33]. Using several patients' and healthy individuals' BALF and PBMC samples, we performed genome-wide RNA-sequencing to characterize the host immune response in COVID-19 patients.…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic characteristics of bronchoalveolar lavage fluid and peripheral blood mononuclear cells in COVID-19 patients

Xiong

Liu

Cao

et al. 2020

Emerging Microbes & Infections

1,089

1,031

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Section: Discussionmentioning

confidence: 99%

Transcriptomic characteristics of bronchoalveolar lavage fluid and peripheral blood mononuclear cells in COVID-19 patients

Xiong

Liu

Cao

et al. 2020

Emerging Microbes & Infections

1,089

1,031

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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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“…Our knowledge about the host immune interaction with SARS-CoV-2 is restricted, making it more di cult for management and developing new therapies. Viral infection typically induces massive changes in the transcriptome of the host, resulting in aberration of host cells' metabolism and modulation of immune response, toward enhancing viral replication [16,17]. Using several samples expression data from human lung epithelial cells including independent biological triplicates of primary human lung epithelium (NHBE) and transformed lung alveolar (A549) cells, we performed transcriptome analysis to better understand the molecular basis of the COVID-19 and identify putative markers.…”

Section: Discussionmentioning

confidence: 99%

Transcriptional analysis of lung epithelial cells using WGCNA revealed the role of IRF9 and IFI6 genes in SARS-CoV-2 pathogenicity

Karami

Derakhshani

Fereidouni

et al. 2020

Preprint

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The coronavirus disease 2019 (COVID-19) outbreak is an ongoing global health emergence, but the pathogenesis remains unclear. Here, we applied weighted gene co-expression network analysis to comprehensively characterize transcriptional changes in bronchial epithelium cells (NHBE and A549 cells) during SARS-CoV-2 infection. Our analysis identified a network highly correlated to COVID-19 pathogenicity based on MX1, IFIT1, ISG15, IFI6, DDX60, IRF9, PARP9, PGLYRP4, IL36G, SAA2 and IL-8 hub genes. The results also indicated a unique transcriptional signatures of infected cells including IFI6 and IRF9 as novel gene candidates and suggested their prospective mechanism in COVID-19 pathogenesis. The result of hub genes enrichment showed that the most correlation topic in biological process and KEGG were type I interferon signaling pathway, IL-17 signaling pathway, cytokine mediated signaling pathway, and defense response to virus categories which all play significant roles in restricting viral infection. Also according to the drug-target network, we recognized 54 FDA-approved drug candidates for other indications could potentially use for the treatment of COVID-19 patients through regulation of six hub genes of the co-expression network. Our findings also showed that the 19 experimentally validated miRNAs regulated the co-expression network through 5 hub genes (SLC19A3, FAM13A, PLA2G16, and HRASLS5). In conclusion, these hub genes had potential roles in the translational medicine and might become promising therapeutic targets further in vitro and in vivo experimental studies are needed to evaluate the role of above mentioned genes in COVID-19.

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Viral hijacking of cellular metabolism

Cited by 392 publications

References 153 publications

Transcriptomic characteristics of bronchoalveolar lavage fluid and peripheral blood mononuclear cells in COVID-19 patients

Transcriptomic characteristics of bronchoalveolar lavage fluid and peripheral blood mononuclear cells in COVID-19 patients

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

Transcriptional analysis of lung epithelial cells using WGCNA revealed the role of IRF9 and IFI6 genes in SARS-CoV-2 pathogenicity

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