scholarly journals In vivo suppression of injury-induced vascular smooth muscle cell accumulation using adenovirus-mediated transfer of the herpes simplex virus thymidine kinase gene.

1994 ◽  
Vol 91 (22) ◽  
pp. 10732-10736 ◽  
Author(s):  
R. J. Guzman ◽  
E. A. Hirschowitz ◽  
S. L. Brody ◽  
R. G. Crystal ◽  
S. E. Epstein ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Thymidine Kinase Gene ◽  
Kinase Gene ◽  
Cell Accumulation ◽  
Simplex Virus

scholarly journals Inhibition of Rat Vascular Smooth Muscle Cell Proliferation In Vitro and In Vivo by Recombinant Replication-Competent Herpes Simplex Virus

Stroke ◽  
1999 ◽  
Vol 30 (11) ◽  
pp. 2431-2439 ◽  
Author(s):  
Shin-Ichi Miyatake ◽  
Hiroyuki Yukawa ◽  
Hiroki Toda ◽  
Norihiro Matsuoka ◽  
Rei Takahashi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Simplex Virus ◽  
Proliferation In Vitro

scholarly journals Adenoviral-Mediated Herpes Simplex Virus-Thymidine Kinase Gene Transfer in Vivo for Treatment of Experimental Human Melanoma

1996 ◽  
Vol 106 (6) ◽  
pp. 1163-1168 ◽  
Author(s):  
Bernd Bonnekoh ◽  
David A. Greenhalgh ◽  
Donnie S. Bundman ◽  
Ken-ichiro Kosai ◽  
Shu-Hsia Chen ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Gene Transfer ◽  
Thymidine Kinase ◽  
Human Melanoma ◽  
Thymidine Kinase Gene ◽  
Kinase Gene ◽  
Simplex Virus

In vivo imaging of herpes simplex virus type 1 thymidine kinase gene expression: early kinetics of radiolabelled FIAU

2000 ◽  
Vol 27 (3) ◽  
pp. 283-291 ◽  
Author(s):  
Roland Haubner ◽  
Norbert Avril ◽  
Petros A. Hantzopoulos ◽  
Bernd Gansbacher ◽  
Markus Schwaiger
Keyword(s):  
Gene Expression ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
In Vivo Imaging ◽  
Thymidine Kinase Gene ◽  
Kinase Gene ◽  
Simplex Virus ◽  
Kinetics Of

Molecular mechanism for ganciclovir resistance in human T lymphocytes transduced with retroviral vectors carrying the herpes simplex virus thymidine kinase gene

Blood ◽  
2001 ◽  
Vol 97 (1) ◽  
pp. 122-129 ◽  
Author(s):  
Marina I. Garin ◽  
Elaine Garrett ◽  
Pierre Tiberghien ◽  
Jane F. Apperley ◽  
David Chalmers ◽  
...  
Keyword(s):  
T Cells ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Marker Gene ◽  
Retroviral Vectors ◽  
Thymidine Kinase Gene ◽  
Kinase Gene ◽  
Donor T Cells ◽  
Simplex Virus

Abstract The herpes simplex virus thymidine kinase gene type 1 (HSV-Tk) ganciclovir (GCV) system is a novel therapeutic strategy for the modulation of graft-versus-host disease (GVHD), a major complication of allogeneic stem cell transplantation (allo-SCT). Retroviral-mediated gene transfer of the HSV-Tk gene into donor T lymphocytes before allo-SCT may allow their in vivo selective depletion after treatment with GCV. The expression of theHSV-Tk gene was analyzed in vitro in CEM cells, a human lymphoblastoid cell line, transduced with 2 different vectors, each containing the HSV-Tk gene and a selectable marker gene. GCV-resistant clones were identified within the clones expressing the marker gene. Characterization of the molecular events leading to this resistance revealed a 227-bp deletion in the HSV-Tk gene due to the presence of cryptic splice donor and acceptor sites within the HSV-Tk gene sequence. Furthermore, it was confirmed that this deletion was present in human primary T cells transduced with either vector and in 12 patients who received transduced donor T cells, together with a T-cell–depleted allo-SCT. In vivo circulating transduced T cells containing the truncated HSV-Tk gene were identified in all patients immediately after infusion and up to 800 days after transplantation. In patients who received GCV as treatment for GVHD, a progressive increase in the proportion of transduced donor T cells carrying the deleted HSV-Tkgene was observed. These results suggest that the limitations within the HSV-Tk/GCV system can be improved by developing optimized retroviral vectors to ensure maximal killing ofHSV-Tk–transduced cells.

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