We previously developed a higher throughput assay of neutralizing antibody to herpes simplex viruses 1 and 2 (Blevins et al., PLOS ONE, 10(12), e0144738) using the enzyme-linked virus inducible system (ELVIS) cell line; this cell line produces β-galactosidase in response to HSV infection.
To analyse gene silencing mechanisms and assess if potential pharmacological treatment affects gene silencing kinetics we transduced U937 myelomonocytic cells with a bicistronic retroviral construct carrying the herpes simplex virus thymidine kinase (HSV-TK) and beta-galactosidase (Lac-Z) genes.
Epstein-Barr virus (EBV)-based and conventional plasmid vectors were constructed that possess the beta-galactosidase (beta-gal) or herpes simplex virus-1 (HSV-1) thymidine kinase (Tk) genes as well as tandem repeats of the human genomic sequence -82 to -42 bp from the transcriptional start site of the CEA gene.
We utilized a replication-defective adenoviral construct containing the beta-galactosidase gene as a control and the herpes simplex virus thymidine kinase gene as the therapeutic vector under the transcription control of the Rous sarcoma virus long terminal repeat promoter.
To target disseminated tumors in vivo, transgenes [beta-galactosidase gene, green fluorescence protein (GFP) gene, herpes simplex virus thymidine kinase (HSV-TK)] were conjugated to transferrin (Tf) by a biotin-streptavidin bridging, which is stoichiometrically controllable, and Tf receptor (Tf-R) affinity chromatography, which selects Tf conjugates with intact receptor bindings sites from reacting with the linker.
Pituitary hormone promoters (human GH or glycoprotein hormone alpha-subunit) were used to express either a marker gene [beta-galactosidase (beta-gal)] or a toxic gene [herpes simplex virus thymidine kinase (TK)].
The ELVIS HSV Id test kit (an enzyme-linked virus-inducible system) (Diagnostic Hybrids, Inc.) uses genetically engineered BHK cells to produce a detectable enzyme, beta-galactosidase, upon infection with either herpes simplex virus (HSV) type 1 (HSV-1) or HSV-2.
Human chondrosarcoma cells (HCS-TG) were transduced with the gene for a herpes simplex virus thymidine kinase (HSV-tk) or Escherichia coli beta-galactosidase (lacZ).
Here, we have generated Moloney murine leukemia virus-derived retroviral vectors co-displaying an anti-CEA scFv-envelope chimeric protein and an unmodified envelope protein to deliver a gene for herpes simplex virus thymidine kinase (HSV-tk) or Escherichia coli beta-galactosidase.
In vitro, human and rabbit keratocytes were transduced with retroviral vectors bearing beta-galactosidase or HStk (herpes simplex virus thymidine kinase) genes.
In anticipation of developing gene therapy against this thyroid carcinoma model, we (1) tested whether adenovirus containing the beta-galactosidase gene could infect FRTL-5 cells and neonatal rat thyroid and (2) evaluated the ability to kill FRTL-5 cells by transfecting them with a transgene in which the thyroglobulin promoter (TG) directed the expression of herpes simplex virus type I thymidine kinase (HSV1TK) and treating TG-HSV1TK-transfected cells with 5 micrograms/ml ganciclovir.
SCID mice were orthotopically transplanted with human ovarian carcinoma cells and, after establishment of tumor, given a recombinant adenovirus expressing either the herpes simplex virus thymidine kinase or the Escherichia coli beta-galactosidase gene.
Here we demonstrate that replication defective recombinant adenoviral vectors, containing the DF3 promoter (bp -725 to +31), can be used to express beta-galactosidase (Ad.DF3-betagal) and the herpes simplex virus thymidine kinase (HSV-tk) gene (Ad.Df3-tk) in DF3 positive breast carcinoma cell lines.
The antigenic and immunogenic potential was examined of human adenovirus type 5 (Ad) recombinants carrying and expressing from one to four tandem repeats of a linear neutralizing epitope from the gD protein of herpes simplex virus type 1 (HSV-1) as a fusion with the beta-galactosidase protein.