TUESDAY, March 31 (HealthDay News) -- Expression of a virion protein called VP16 appears to be necessary for herpes simplex virus to exit its latent state, according to research published in the March issue of PLoS Pathogens.
Richard L. Thompson, Ph.D., of the University of Cincinnati School of Medicine, Ohio, and colleagues used a mouse model of ocular herpes simplex virus pathogenesis along with viral mutants to assess latency and exit from latency at a neuronal level.
The investigators found that in the acute infectious stage in neurons, de novo synthesis of VP16 is needed for viral replication. However, VP16 may not travel well to the nucleus of neurons, which could explain why latency is common in those infected. In order for the virus to leave the latent state, new expression of VP16 is mandatory, the authors write.
"Using new approaches we
now demonstrate that the transactivating function of VP16 is indeed requisite for herpes simplex virus reactivation in vivo. The functional requirement for VP16 is very early in the transition from the latent to the lytic cycle, as in its absence the latent viral genome cannot advance to the production of lytic viral proteins. In contrast, elimination of 'immediate early' and 'early' viral functions previously considered critical for the initiation of reactivation has no measurable effect on lytic viral protein expression at this early stage in reactivation," the authors write.
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