During ZIKV infection, the SUMOylation of NS5 at Lys 252 promotes NS5 NB interactions with STAT2, further disrupting the antiviral promyelocytic leukemia(PML)-STAT2 NBs, promoting PML degradation, and inhibiting the interferon-stimulated gene response, which finally results in the persistent infection of human brain microvascular endothelial cells [10]. Here, STAT2 is linked to Zika virus infectious disease.