Conversely, ECTVΔvSlfn and ECTV-vSlfnΔp26 were completely impaired for such inhibition because infection with both mutant viruses showed notably high levels of STING, TBK1, and IRF3 phosphorylation and STING dimerization, indicative of activation of the cGAS-STING axis (Fig. 2, A and D). Here, TBK1 is linked to infection.