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Significance STING (stimulator of IFN genes) and IFI16 are sensors of DNA in cytoplasm and the nucleus, respectively. Both signal activation of innate immune responses. Both proteins are stable in wild-type virus-infected cells. The key finding with broad implications is that in HSV-1–infected cells STING and IFI16 are actively stabilized inasmuch as they are degraded in cells lacking functional ICP0 or protein kinase US3. Moreover, STING was required for optimal replication in HEp-2 or HeLa cells derived from cancers but was inimical in HEL or HEK293 cells derived initially from normal tissues and in the case of HEK293 cells transformed with viral oncogenes. The requirements for stabilization of STING and IFI16 were not covariant.

HSV-1 degrades, stabilizes, requires, or is stung by STING depending on ICP0, the US3 protein kinase, and cell derivation