Neal A. Deluca

The initiator element in a herpes simplex virus type 1 late-gene promoter enhances activation by ICP4, resulting in abundant late-gene expression.

Expression of herpes simplex virus ICP0 inhibits the induction of interferon-stimulated genes by viral infection.

Phosphorylation of transcription factor Sp1 during herpes simplex virus type 1 infection.

Temperature-dependent conformational changes in herpes simplex virus ICP4 that affect transcription activation.

Relationship of herpes simplex virus genome configuration to productive and persistent infections.

Treatment of rat gliosarcoma brain tumors by HSV-based multigene therapy combined with radiosurgery.

Differential cellular requirements for activation of herpes simplex virus type 1 early (tk) and late (gC) promoters by ICP4.

Herpes simplex virus 1 has multiple mechanisms for blocking virus-induced interferon production.

Inhibition of DNA repair by a herpes simplex virus vector enhances the radiosensitivity of human glioblastoma cells.

Properties of a herpes simplex virus multiple immediate-early gene-deleted recombinant as a vaccine vector.

DNA-dependent oligomerization of herpes simplex virus type 1 regulatory protein ICP4.

Relaxed repression of herpes simplex virus type 1 genomes in Murine trigeminal neurons.

Binding of ICP4, TATA-binding protein, and RNA polymerase II to herpes simplex virus type 1 immediate-early, early, and late promoters in virus-infected cells.

Stabilized binding of TBP to the TATA box of herpes simplex virus type 1 early (tk) and late (gC) promoters by TFIIA and ICP4.

Oligomerization of ICP4 and rearrangement of heat shock proteins may be important for herpes simplex virus type 1 prereplicative site formation.

Therapeutic efficacy of a herpes simplex virus with radiation or temozolomide for intracranial glioblastoma after convection-enhanced delivery.

Epigenetic modulation of gene expression from quiescent herpes simplex virus genomes.

Reversal of heterochromatic silencing of quiescent herpes simplex virus type 1 by ICP0.

Activities of ICP0 involved in the reversal of silencing of quiescent herpes simplex virus 1.

Herpes simplex virus 1 ICP4 forms complexes with TFIID and mediator in virus-infected cells.

The N terminus and C terminus of herpes simplex virus 1 ICP4 cooperate to activate viral gene expression.

Nuclear IFI16 induction of IRF-3 signaling during herpesviral infection and degradation of IFI16 by the viral ICP0 protein.

Requirement of the N-terminal activation domain of herpes simplex virus ICP4 for viral gene expression.

Temporal association of herpes simplex virus ICP4 with cellular complexes functioning at multiple steps in PolII transcription.

Transcription of the herpes simplex virus 1 genome during productive and quiescent infection of neuronal and nonneuronal cells.

Selective recruitment of nuclear factors to productively replicating herpes simplex virus genomes.

History and genomic sequence analysis of the herpes simplex virus 1 KOS and KOS1.1 sub-strains.

Production of immunogenic West Nile virus-like particles using a herpes simplex virus 1 recombinant vector.

Replication-Coupled Recruitment of Viral and Cellular Factors to Herpes Simplex Virus Type 1 Replication Forks for the Maintenance and Expression of Viral Genomes.

A Herpesviral Immediate Early Protein Promotes Transcription Elongation of Viral Transcripts.