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Significance To shed light on the host range of Zika virus (ZIKV), we surveyed the virus’ ability to infect cells of evolutionarily diverse species. ZIKV replicates efficiently in human, great ape, Old and New World monkey, but not rodent cells. These observations correlated with ZIKV’s ability to blunt the cGAS/STING signaling pathway in all primate cells tested but not in mice. We demonstrate that an enzyme shared by many flaviviruses (NS2B3) is responsible for functionally inactivating this antiviral defense. Our results highlight the importance of the cGAS/STING pathway in shaping the host range of ZIKV, which in turn may guide the development of murine models with inheritable susceptibility to ZIKV and other flaviviruses.

Species-specific disruption of STING-dependent antiviral cellular defenses by the Zika virus NS2B3 protease