Cell 174, 1143–1157 (2018)

Pox viruses are cytosolic DNA viruses, yet they do not activate cytosolic DNA sensors. In Cell, Meade et al. identify a conserved pox virus–encoded protein, F17, that indirectly disrupts sensing by host cGAS and impedes activation of the STING-dependent pathway. F17 competitively binds to Raptor and Rictor and displaces both from mTOR. Rather than impairing mTOR’s activity, F17 induces a hyper-activated mTOR state needed for the synthesis of late viral proteins. Concurrently, this dysregulated mTOR localizes to the Golgi, contributing to destabilization of cGAS to suppress the induction of antiviral type I interferon responses. F17 thus mediates viral immune evasion.