How the viral DNA sensors are optimally activated to establish efficient innateimmunity to viruses at the early phase of infection and then timely turned off at thelate phase to avoid immune damage is enigmatic. We found that these viral DNAsensors are dynamically and temporally regulated by post-translational modificationssuch sumoylation and polyubiquitination by common and distinct mechanisms. Ourfindings reveal the delicate mechanisms that ensure proper innate immunity toviruses and provide potential targets for drug development against infectious andautoimmune diseases.
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