A tunable immune-evasion function of Zika virus NS5 governs viral fitness and pathogenesis

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE344436 | GEO | 2026/08/20

REPOSITORIES: GEO