Relaxed Repression of Herpes Simplex Virus Type 1 Genomes in Murine Trigeminal Neurons

We ini- tially tested the ICP0 promoter because ICP0 expression stim- ulates reactivation from latency ( 8–10 ), the ICP0 promoter is stimulated by hyperthermic stress ( 31 ), and

In the present study, we identified a novel function of HSV-1 VP22, namely, regulation of the proper subcellular localization of viral proteins VP16, VP26, ICP0, ICP4, and ICP27

Likewise, in cells infected with HSV-1 expressing the C-terminal half of VP22, which we have shown above does not complex with ICP0 but is packaged into the virus, ICP0 local-

In contrast, VP16, ICP0, HSV-1 transcription, spe- cific HSV-1 proteins, or genome replication is required to enhance the basal mobilization of H1.2 and to increase its free pool..

The transgenic ICP4 promoter is activated in Schwann cells but not neurons in trigeminal ganglia of transgenic mice latently infected with HSV-1.. Transgenic mice were infected

This mutant effectively lacks functional VP16, ICP0, and ICP4 upon infection of cells at 38.5°C (43), thereby providing a means of analyzing the intrinsic activities of promoters

Vero cells were biochemically transformed with the gene encoding ICP4 of herpes simplex virus type 2 (HSV-2).. These cells were used as permissive hosts to isolate and propagate

HSV-2 glycoproteins immunoprecipitated by antiserum R#5 in the absence or presence of various amounts of unlabeled extract from HEp-2 cells infected with HSV-1(mP) or