Herpes simplex virus type 1-based amplicon vectors for fundamental research in neurosciences and gene therapy of neurological diseases

2012 ◽  
Vol 106 (1-2) ◽  
pp. 2-11 ◽  
Author(s):  
Diana Jerusalinsky ◽  
María Verónica Baez ◽  
Alberto Luis Epstein
Keyword(s):  
Gene Therapy ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Neurological Diseases ◽  
Fundamental Research ◽  
Simplex Virus

PD9-07 HERPES SIMPLEX VIRUS TYPE-1 (HSV-1) VECTOR-MEDIATED GENE THERAPY OF ENDOMORPHIN FOR BLADDER OVERACTIVITY AND NOCICEPTION

2014 ◽  
Vol 191 (4S) ◽  
Author(s):  
Hiroki Okada ◽  
Darren Wolfe ◽  
James Wechuck ◽  
James R. Goss ◽  
Tsuyoshi Majima ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Simplex Virus ◽  
Hsv 1

scholarly journals Adenovirus-Mediated Herpes Simplex Virus Type-1 Thymidine Kinase Gene Therapy Suppresses Oestrogen-Induced Pituitary Prolactinomas*

2000 ◽  
Vol 85 (3) ◽  
pp. 1296-1305 ◽  
Author(s):  
S. Windeatt ◽  
T. D. Southgate ◽  
R. A. Dewey ◽  
F. Bolognani ◽  
M. J. Perone ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Cell Line ◽  
Thymidine Kinase ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Simplex Virus ◽  
Plasma Prl

AbstractWe tested the hypothesis that gene transfer using recombinant adenovirus vectors (RAds) expressing herpes simplex virus type 1 thymidine kinase (HSV1-TK) might offer an alternative therapeutic approach for the treatment of pituitary prolactinomas that do not respond to classical treatment strategies. HSV1-TK converts the prodrug ganciclovir (GCV) to GCV monophosphate, which is in turn further phosphorylated by cellular kinases to GCV triphosphate, which is toxic to proliferating cells. One attractive feature of this system is the bystander effect, whereby untransduced cells are also killed. Our results show that RAd/HSV1-TK in the presence of GCV is nontoxic for the normal anterior pituitary (AP) gland in vitro, but causes cell death in the pituitary tumor cell lines GH3, a PRL/GH-secreting cell line, and AtT20, a corticotrophic cell line. We have used sulpiride- and oestrogen-induced lactotroph hyperplasia within the rat AP gland as an in vivo animal model. Intrapituitary infection of rats bearing oestrogen-induced lactotroph hyperplasia, with RAd/HSV1-TK and subsequent treatment with GCV, decreases plasma PRL levels and reduces the mass of the pituitary gland. More so, there were no deleterious effects on circulating levels of other AP hormones, suggesting that the treatment was nontoxic to the AP gland in situ. In summary, our results show that suicide gene therapy using the HSV1-TK transgene could be further developed as a useful treatment to complement current therapies for prolactinomas.

Biosafety of Gene Therapy Vectors Derived From Herpes Simplex Virus Type 1

2014 ◽  
Vol 13 (6) ◽  
pp. 478-491 ◽  
Author(s):  
Filip Lim ◽  
Hena Khalique ◽  
Maria Ventosa ◽  
Aline Baldo
Keyword(s):  
Gene Therapy ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Gene Therapy Vectors ◽  
Simplex Virus

Use of herpes simplex virus type 1 for transgene expression within the nervous system*

1999 ◽  
Vol 96 (6) ◽  
pp. 533-541 ◽  
Author(s):  
Robin H. LACHMANN ◽  
Stacey EFSTATHIOU
Keyword(s):  
Gene Therapy ◽  
Nervous System ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Viral Genome ◽  
Latently Infected ◽  
Simplex Virus

Gene therapy might provide a useful treatment for a number of neurological diseases and a great deal of effort is going into the development of vector systems which will allow the delivery of potentially therapeutic genes to terminally differentiated neurons within the intact mammalian brain. The ability of herpes simplex virus type 1 (HSV-1) to establish a lifelong latent infection within neurons has led to interest in its use as a neuronal gene delivery vector. During HSV latency no viral proteins are produced and transcription from the latent viral genome is limited to a family of nuclear RNAs, the latency-associated transcripts, whose function is not well understood. Obtaining prolonged expression of a transgene in latently infected neurons has proven difficult due to transcriptional silencing of exogenous promoters introduced into the latent viral genome. For this reason there is a great deal of interest in utilizing the HSV latency-associated promoter to drive the expression of therapeutic genes in latently infected neurons of both the peripheral and central nervous systems. In this review we describe a strategy which allows the latency-associated promoter to drive long-term reporter gene expression in the mammalian nervous system. These observations open up the possibility of using similar HSV-based vectors to express therapeutic transgenes within the brain and investigate the potential of gene therapy in a range of neurological disorders.

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