Deficiency of HIF-1α enhances influenza A virus replication by promoting autophagy in alveolar type II epithelial cells
Caiqi Zhao, Jie Chen, Lianping Cheng, Kai‐Feng Xu, Yiyu Yang, Xiao Su
Abstract
reduced glycolysis by regulating transcription of glycolysis-related enzymes, which subsequently activated the AMPKα-ULK1 signalling pathway. Interestingly, AMPKα-ULK1 signalling promoted autophagy and augmented IAV replication. Taken together, deficiency of HIF-1α in lung epithelial cells reduces glycolysis and enhances AMPKα-ULK1-mediated autophagy, which finally facilitates IAV replication. These findings have deepened our understanding of the role of HIF-1α in regulating IAV replication and provided us novel therapeutic targets for combating influenza infection.
Topics & Concepts
AMPKAutophagyInfluenza A virusGene knockdownBiologyViral replicationInflammationCell biologyHIF1ACancer researchImmunologyVirusCell cultureKinaseProtein kinase AApoptosisAngiogenesisGeneticsBiochemistryCancer, Hypoxia, and MetabolismAutophagy in Disease and TherapyRNA modifications and cancer