{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE298nnn/GSE298514/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE298514"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Vanin-1 deficiency enhances host tolerance to influenza infection by modulating cellular redox status","description":"Host survival during infection depends on the balance between pathogen resistance and tissue tolerance mechanisms. Although resistance pathways are well-characterized, the molecular determinants of host tolerance remain poorly understood. Here we demonstrate that vanin-1, an ectoenzyme known for its role in vitamin B5 metabolism, unexpectedly regulates host tolerance during influenza infection through modulation of cellular redox status. Mice lacking vanin-1 showed enhanced survival following lethal influenza infection without alterations in viral burden, immune responses, or tissue pathology. While vanin-1 deficiency impairs vitamin B5 metabolism, neither vitamin B5 supplementation nor deficiency affected survival during infection, indicating a vitamin B5- independent mechanism. RNA sequencing analysis revealed enhanced expression of antioxidant pathway genes in vanin-1-deficient mice, with Nrf2 serving as a key upstream regulator. Mechanistically, vanin-1-deficient mice maintained higher glutathione levels during infection and showed reduced lipid peroxidation, suggesting protection against oxidative stress-induced cell death. Importantly, pharmacological inhibition of glutathione synthesis abolished the survival advantage in vanin-1-deficient mice, while glutathione supplementation protected wild-type mice from lethal infection. Our findings reveal an unexpected role for vanin-1 in regulating host tolerance through antioxidant pathways and identify a potential therapeutic target for enhancing survival during severe viral infections.","dates":{"publication":"2026/06/22"},"accession":"GSE298514","cross_references":{"GSM":["GSM9015947","GSM9015948","GSM9015949","GSM9015950","GSM9015951","GSM9015952","GSM9015953","GSM9015954","GSM9015955","GSM9015956","GSM9015957","GSM9015946"],"GPL":["34290"],"GSE":["298514"],"taxon":["Mus musculus"],"PMID":["[42369873]"]}}