«ul39»

Developing oncolytic Herpes simplex virus type 1 through UL39 knockout by CRISPR-Cas9

Objective(s): Oncolytic Herpes simplex virus type 1 (HSV-1) has emerged as a promising strategy for cancer therapy. However, development of novel oncolytic mutants has remained a major challenge owing to low efficiency of conventional genome editing methods. Recently, CRISPR-Cas9

Sequence Analysis of the UL39, UL38, and UL37 Homologues of Bovine Herpesvirus 1 and Expression Studies of UL40 and UL39, the Subunits of Ribonucleotide Reductase

Herpes Simplex Virus 1 Mutant with Point Mutations in UL39 Is Impaired for Acute Viral Replication in Mice, Establishment of Latency, and Explant-Induced Reactivation

Flip-Flop HSV-BAC: bacterial artificial chromosome based system for rapid generation of recombinant herpes simplex virus vectors using two independent site-specific recombinases

BACKGROUND Oncolytic herpes simplex virus (HSV) vectors that specifically replicate in and kill tumor cells sparing normal cells are a promising cancer therapy. Traditionally, recombinant HSV vectors have been generated through homologous recombination between the HSV genome and

Simplex Virus Type 1 Expressing the Prodrug-Activating Brain Tumor Oncolysis with Replication-Conditional Herpes

The treatment of malignant glioma is currently ineffective. Oncolytic viruses are being explored as a means to selectively lyse tumor cells in the brain. We have engineered a mutant herpes simplex virus type 1 with deletions in the viral UL39 and g134.5 genes and an insertion of

B-myb promoter retargeting of herpes simplex virus gamma34.5 gene-mediated virulence toward tumor and cycling cells.

Deletion of the gamma34.5 gene coding for virulence markedly reduces cytotoxicity mediated by herpes simplex virus type 1 (HSV-1) (J. M. Markert et al., Neurosurgery 32:597-603, 1993; N. S. Markovitz et al. , J. Virol. 71:5560-5569, 1997). To target lytic virulence to tumors, we

Comparative full-length sequence analysis of oncogenic and vaccine (Rispens) strains of Marek's disease virus.

The complete DNA sequence of the Marek's disease virus serotype 1 vaccine strain CVI988 was determined and consists of 178 311 bp with an overall gene organization identical to that of the oncogenic strains. In examining open reading frames (ORFs), nine differ between vaccine and

Cancer Therapy: Preclinical A Novel Oncolytic Herpes Simplex Virus that Synergizes with Phosphoinositide 3-kinase/Akt Pathway Inhibitors to Target Glioblastoma Stem Cells

Purpose: To develop a new oncolytic herpes simplex virus (oHSV) for glioblastoma (GBM) therapy that will be effective in glioblastoma stem cells (GSC), an important and untargeted component of GBM. One approach to enhance oHSV efficacy is by combination with other therapeutic mod

Reduction of herpes simplex virus type-2 replication in cell cultures and in rodent models with peptide-conjugated morpholino oligomers.

BACKGROUND Genital herpes, caused by herpes simplex virus type-2 (HSV-2), is a recurrent, lifelong disease affecting tens of millions of people in the USA alone. HSV-2 can be treated therapeutically with acyclovir (ACV) and its derivatives; however, no treatment can prevent HSV r

Oncolytic herpes simplex virus mutants exhibit enhanced replication in glioma cells evading temozolomide chemotherapy through deoxyribonucleic acid repair.

INTRODUCTION Engineered oncolytic viruses take advantage of cancer cell mutations and induce selective destruction.1–3 We hypothesized that chemotherapy-induced tumor-protective deoxyribonucleic acid (DNA) repair proteins promote oncolytic herpes simplex virus (HSV) replication.