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The γ1 34.5 protein of herpes simplex viruses (HSV) is essential for virulence. Accordingly, an HSV mutant lacking γ1 34.5 is attenuatedin vivo . Despite its vaccine potential, the mechanism by which the γ1 34.5 null mutant triggers protective immunity is unknown. In this report we show that vaccination with the γ1 34.5 null mutant protects against lethal challenge from wild-type virus via IκB kinase in dendritic cells (DCs), which sense virus-associated molecular patterns. Unlike mock-treated DCs, DCs primed with the γ1 34.5 null mutantex vivo mediate resistance to wild-type HSV after adoptive transfer into naïve mice. Furthermore, the γ1 34.5 null mutant activates IκB kinase, which facilitates p65/RelA phosphorylation and nuclear translocation, resulting in DC maturation. While unable to produce infectious virus in DCs, this mutant virus expresses early and late genes. In its abortive infection, the γ1 34.5 null mutant induces protective immunity more effectively in CD8+ DCs than in CD8− DCs. This is mirrored by a higher level of interleukin-6 (IL-6) and IL-12 secretion by CD8+ DCs than CD8− DCs. Remarkably, inhibition of p65/RelA phosphorylation or nuclear translocation in CD8+ DCs disrupts protective immunity. These results suggest that engagement of the γ1 34.5 null mutant with CD8+ DCs elicits innate immunity to activate NF-κB, which translates into protective immunity.

journal of virology

Activation of NF-κB in CD8 + Dendritic Cells Ex Vivo by the γ 1 34.5 Null Mutant Correlates with Immunity against Herpes Simplex Virus 1