De Novo Synthesis of VP16 Coordinates the Exit from HSV Latency In Vivo (original) (raw)
Figure 7
The regulation of expression of VP16 controls the balance between lytic and latent infection of sensory neurons at all stages of the virus infection cycle.
(A) Shown is a schematic of the role of de novo VP16 expression during acute infection of the trigeminal ganglion. As detailed in the text, we hypothesize that VP16 protein is not transported efficiently to neuronal cell bodies and that sequences present in the VP16 promoter direct the de novo expression of VP16, which overcomes repressors (e.g. riboregulators) to initiate lytic infection during the acute stage of viral replication. (B) We hypothesize that following stress the de novo synthesis of VP16 initiates a feedback loop with the IE genes that results in viral reactivation in one or a very few of the 6,000 latently infected neurons present in the ganglion.