{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kalugotla G"],"funding":["National Institute of Allergy and Infectious Diseases","NIAID NIH HHS","Burroughs Wellcome Fund","NCI NIH HHS","National Institute of General Medical Sciences","NIGMS NIH HHS"],"pagination":["e1012900"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12646485"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(11)"],"pubmed_abstract":["Autophagy is an essential cellular process which functions to maintain homeostasis in response to stressors such as starvation or infection. Here, we report that a subset of autophagy factors including ATG-3 play an antiviral role in Orsay virus infection of Caenorhabditis elegans. Orsay virus infection does not modulate autophagic flux, and re-feeding after starvation limits Orsay virus infection and blocks autophagic flux, suggesting that the role of ATG-3 in Orsay virus susceptibility is independent of its role in maintaining autophagic flux. atg-3 mutants phenocopy rde-1 mutants, which have a defect in RNA interference (RNAi), in susceptibility to Orsay virus infection and transcriptional response to infection. However, atg-3 mutants do not exhibit defects in RNAi. Additionally, ATG-3 "],"journal":["PLoS pathogens"],"pubmed_title":["ATG-3 limits Orsay virus infection in C. elegans and regulates collagen pathways."],"pmcid":["PMC12646485"],"funding_grant_id":["R01 AI173360","P30 CA091842","R35 GM152192","T32 AI007163","T32 GM007200","Investigator in the Pathogenesis of Infectious Disease"],"pubmed_authors":["Schriefer LA","Kalugotla G","Perez LC","Morrison SA","Marmerstein V","Schedl T","Pak SC","Baldridge MT","Silverman GA","Wang L"],"additional_accession":[]},"is_claimable":false,"name":"ATG-3 limits Orsay virus infection in C. elegans and regulates collagen pathways.","description":"Autophagy is an essential cellular process which functions to maintain homeostasis in response to stressors such as starvation or infection. Here, we report that a subset of autophagy factors including ATG-3 play an antiviral role in Orsay virus infection of Caenorhabditis elegans. Orsay virus infection does not modulate autophagic flux, and re-feeding after starvation limits Orsay virus infection and blocks autophagic flux, suggesting that the role of ATG-3 in Orsay virus susceptibility is independent of its role in maintaining autophagic flux. atg-3 mutants phenocopy rde-1 mutants, which have a defect in RNA interference (RNAi), in susceptibility to Orsay virus infection and transcriptional response to infection. However, atg-3 mutants do not exhibit defects in RNAi. Additionally, ATG-3 ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-05-20T03:17:16.527Z","creation":"2026-05-20T03:09:34.698Z"},"accession":"S-EPMC12646485","cross_references":{"pubmed":["41252446"],"doi":["10.1371/journal.ppat.1012900"]}}