Further analysis of the early events in HSV-1 replication in neuronal tissue showed that the levels of HSV-1 in trigeminal ganglia was comparable between WT and STINGgt/gt mice at day 2 post infection, after which we observed significantly elevated viral load in trigeminal ganglia from STING-deficient mice (Supplementary Fig. 2f). This evidence concerns the gene STING1 and infection.