Extended Data Fig. 10: Model for the dual inhibition of innate immunity and apoptosis by HCMV UL37x1.

Left: Apoptotic caspases cleave key components of the cGAS-STING axis to inhibit innate immune signaling. Right: During HCMV infection, UL37x1 inhibits apoptosis, which enhances cGAS-STING immune signaling. On the other hand, UL37x1 can directly target to TBK1 to disrupt TBK1 interaction with STING as well as IRF3 recruitment to STING, thereby suppressing the cGAS-STING pathway. This immunosuppressing activity of UL37x1 counterbalances the immune enhancing “side-effect” of UL37x1’s anti-apoptotic activity.