<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE344nnn/GSE344436/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE344436</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>A tunable immune-evasion function of Zika virus NS5 governs viral fitness and pathogenesis</name><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.</description><dates><publication>2026/08/20</publication></dates><accession>GSE344436</accession><cross_references><GSM>GSM9978960</GSM><GSM>GSM9978962</GSM><GSM>GSM9978961</GSM><GSM>GSM9978964</GSM><GSM>GSM9978963</GSM><GSM>GSM9978966</GSM><GSM>GSM9978965</GSM><GSM>GSM9978968</GSM><GSM>GSM9978967</GSM><GSM>GSM9978959</GSM><GSM>GSM9978958</GSM><GSM>GSM9978969</GSM><GPL>29480</GPL><GSE>344436</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>