The inert meets the living: The expanding view of metabolic alterations during viral pathogenesis

• Published in: PLoS pathogens 2019-07, Vol.15 (7), p.e1007830-e1007830
• Main Authors: Passalacqua, Karla D, Purdy, John G, Wobus, Christiane E
• Format: Article
• Language: English
• Subjects: Amino acids; Animals; Antiviral Agents - metabolism; Apoptosis; Bacterial diseases; Bacterial infections; Biology and Life Sciences; Biomolecules; Carbohydrates; Care and treatment; Cell cycle; Cell Death; Communicable diseases; Communicable Diseases - etiology; Communicable Diseases - metabolism; Disease Progression; Disease Reservoirs - virology; Eating - physiology; Energy storage; Fasting; Fasting - metabolism; Free energy; Health aspects; HIV-1 - metabolism; HIV-1 - pathogenicity; Host Microbial Interactions - physiology; Humans; Immune response; Immunology; Infections; Inflammation; Influenza; Lipid metabolism; Lipids; Medicine and Health Sciences; Metabolic networks; Metabolic pathways; Metabolism; Metabolites; Models, Biological; Nucleotides; Nutrients; Pathogenesis; Pearls; Progeny; Receptors; Risk factors; Scientists; Studies; Succinates - metabolism; Thermodynamics; Tropism; Tumors; Viral infections; Viruses; Viruses - metabolism; Viruses - pathogenicity; Zika virus
• ISSN: 1553-7374; 1553-7366; 1553-7374
• DOI: 10.1371/journal.ppat.1007830

Viruses possess the information-storage characteristic of life but lack the ability to extract free energy from nutrients. [...]viruses require host cell metabolism to perform the work needed for making new viral particles. Because viruses construct viral progeny from stolen biomolecules (e.g., amino acids, nucleotides, and sometimes lipids), the primary tier of research into the virus-host-metabolism relationship has focused on metabolic pathways that provide these needed materials. In this context, it is important to remember that studies about the effects of bacterial infection on mammalian cell metabolism may be confounded by the fact that bacteria are cellular and, unlike viruses, encode a metabolic network, and are confined by their own metabolic constraints. [...]it may be hard to disentangle just whose metabolism is being altered under experimental conditions, making the study of metabolism during viral infection easier to interpret. [...]the traditional paradigm of viewing host cell susceptibility to viral infection in terms of the availability of specific protein/carbohydrate receptors can now be expanded to also include the underlying metabolic behavior of target cells as another host determinant of virus tropism.