Metabolic host response and therapeutic approaches to influenza infection.
Cell Mol Biol Lett
; 25: 15, 2020.
Article
em En
| MEDLINE
| ID: mdl-32161622
ABSTRACT
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 ß-oxidation 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.
Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Interferons
/
Metabolismo Energético
/
Indolamina-Pirrol 2,3,-Dioxigenase
/
Metabolismo dos Lipídeos
/
Influenza Humana
/
Glucose
Limite:
Humans
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Article