{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE344nnn/GSE344436/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE344436"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"A tunable immune-evasion function of Zika virus NS5 governs viral fitness and pathogenesis","description":"Zika virus (ZIKV) nonstructural protein 5 (NS5) antagonizes host antiviral immunity, but how this immune-evasion activity is regulated to support viral fitness and pathogenesis remains incompletely understood. In this study, we investigated the functional importance of NS5 residue L162 by comparing wild-type ZIKV with the ZIKV-NS5L162A and ZIKV-NS5L162G mutants. RNA sequencing was performed in A549 cells that were mock infected or infected with wild-type or mutant ZIKV to characterize virus-induced transcriptional responses and determine how substitutions at NS5 residue L162 alter host gene expression. These data provide a genome-wide resource for defining NS5-dependent regulation of innate immune and antiviral responses.","dates":{"publication":"2026/08/20"},"accession":"GSE344436","cross_references":{"GSM":["GSM9978960","GSM9978962","GSM9978961","GSM9978964","GSM9978963","GSM9978966","GSM9978965","GSM9978968","GSM9978967","GSM9978959","GSM9978958","GSM9978969"],"GPL":["29480"],"GSE":["344436"],"taxon":["Homo sapiens"]}}