{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Doshi H"],"funding":["Landesgraduiertenstipendium","Jena University Hospital IZKF","Deutsche Forschungsgemeinschaft"],"pubmed_abstract":["Herpes simplex virus type 1 (HSV-1) is a widespread contagious pathogen, mostly causing mild symptoms on the mucosal entry side. However, systemic distribution, in particular upon reactivation of the virus in immunocompromised patients, may trigger an innate immune response and induce damage of organs. In these conditions, HSV-1 may infect vascular endothelial cells, but little is known about the regulation of HSV-1 replication and possible defense mechanisms in these cells. The current study addresses the question of whether the host cell protein AMP-activated protein kinase (AMPK), an important metabolic sensor, can control HSV-1 replication in endothelial cells. We show that downregulation of the catalytic subunits AMPKα1 and/or AMPKα2 increased HSV-1 replication as monitored by TCID<su"],"journal":["Microbiology spectrum"],"pagination":["e0041723"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10580915"],"repository":["biostudies-literature"],"pubmed_title":["AMPK protects endothelial cells against HSV-1 replication via inhibition of mTORC1 and ACC1."],"pmcid":["PMC10580915"],"funding_grant_id":["RTG 2155","MSP 11","AMSP 19"],"pubmed_authors":["Oakhill JS","Baell J","Godbole A","Doshi H","Gee YS","Henke A","Spengler K","Heller R"],"additional_accession":[]},"is_claimable":false,"name":"AMPK protects endothelial cells against HSV-1 replication via inhibition of mTORC1 and ACC1.","description":"Herpes simplex virus type 1 (HSV-1) is a widespread contagious pathogen, mostly causing mild symptoms on the mucosal entry side. However, systemic distribution, in particular upon reactivation of the virus in immunocompromised patients, may trigger an innate immune response and induce damage of organs. In these conditions, HSV-1 may infect vascular endothelial cells, but little is known about the regulation of HSV-1 replication and possible defense mechanisms in these cells. The current study addresses the question of whether the host cell protein AMP-activated protein kinase (AMPK), an important metabolic sensor, can control HSV-1 replication in endothelial cells. We show that downregulation of the catalytic subunits AMPKα1 and/or AMPKα2 increased HSV-1 replication as monitored by TCID<su","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Sep","modification":"2026-06-05T04:59:08.942Z","creation":"2025-04-04T11:00:27.283Z"},"accession":"S-EPMC10580915","cross_references":{"pubmed":["37702499"],"doi":["10.1128/spectrum.00417-23"]}}