tetano
Editor, Senior Moderator
Microb Pathog
. 2023 Jan 21;106002.
doi: 10.1016/j.micpath.2023.106002. Online ahead of print.
Comprehensive analysis of lipid metabolism in influenza virus infection
Xiaoyong Chen[SUP] 1 [/SUP], Shuaiwei Wang[SUP] 2 [/SUP], Peiling Gan[SUP] 2 [/SUP], Jianlong Zhang[SUP] 3 [/SUP], Guangzhi Tong[SUP] 4 [/SUP], Suzhen Liu[SUP] 5 [/SUP]
Affiliations
Abstract
Influenza A virus (IAV) exploits host metabolic pathways to support its replication. To improve the understanding of lipid metabolic changes that could occur upon IAV infection, a comprehensive analysis of lipid metabolites in A549 cells infected with the avian H9N2 virus at the different time points was performed. It was found that H9N2 infection could largely promote the level of lipid metabolites. Further, these metabolites were mainly included in glycerophospholipids (GP), sphingolipid (SP), glycerolipids (GL), fatty acid (FA), sterollipids (ST), triglyceride (TG), and prenol lipids (PR). Specifically, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that these metabolites were mainly associated with the glycerphospholipid metabolism, glycosylphosphatidylinositol (GPI)-anchor biosynthesis, and autophagy. Furthermore, it is interesting to note that these metabolites, including FFA(19:1), PE(P-17:0_20:3), PE(P-18:1_20:2), LPC(14:0/0:0), PE(O-18:0_20:3), and MGDG(16:0_18:1), are upregulated and shared in the top 10 at 12 h, 24 h, 36 h, and 48 h after H9N2 infection, indicative of the possibility of acting as biomarkers for the diagnosis in the lung infected with influenza virus. These pathways and altered metabolites could provide new understandings about biological characteristics and pathogenicity of influenza virus and have the potential to serve as biomarkers for influenza.
Keywords: Influenza virus; Lipid metabolites; Metabolic pathways.
. 2023 Jan 21;106002.
doi: 10.1016/j.micpath.2023.106002. Online ahead of print.
Comprehensive analysis of lipid metabolism in influenza virus infection
Xiaoyong Chen[SUP] 1 [/SUP], Shuaiwei Wang[SUP] 2 [/SUP], Peiling Gan[SUP] 2 [/SUP], Jianlong Zhang[SUP] 3 [/SUP], Guangzhi Tong[SUP] 4 [/SUP], Suzhen Liu[SUP] 5 [/SUP]
Affiliations
- PMID: 36693511
- DOI: 10.1016/j.micpath.2023.106002
Abstract
Influenza A virus (IAV) exploits host metabolic pathways to support its replication. To improve the understanding of lipid metabolic changes that could occur upon IAV infection, a comprehensive analysis of lipid metabolites in A549 cells infected with the avian H9N2 virus at the different time points was performed. It was found that H9N2 infection could largely promote the level of lipid metabolites. Further, these metabolites were mainly included in glycerophospholipids (GP), sphingolipid (SP), glycerolipids (GL), fatty acid (FA), sterollipids (ST), triglyceride (TG), and prenol lipids (PR). Specifically, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that these metabolites were mainly associated with the glycerphospholipid metabolism, glycosylphosphatidylinositol (GPI)-anchor biosynthesis, and autophagy. Furthermore, it is interesting to note that these metabolites, including FFA(19:1), PE(P-17:0_20:3), PE(P-18:1_20:2), LPC(14:0/0:0), PE(O-18:0_20:3), and MGDG(16:0_18:1), are upregulated and shared in the top 10 at 12 h, 24 h, 36 h, and 48 h after H9N2 infection, indicative of the possibility of acting as biomarkers for the diagnosis in the lung infected with influenza virus. These pathways and altered metabolites could provide new understandings about biological characteristics and pathogenicity of influenza virus and have the potential to serve as biomarkers for influenza.
Keywords: Influenza virus; Lipid metabolites; Metabolic pathways.