herpes simplex/hypoxia

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Herpes simplex virus amplicon delivery of a hypoxia-inducible soluble vascular endothelial growth factor receptor (sFlk-1) inhibits angiogenesis and tumor growth in pancreatic adenocarcinoma.

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BACKGROUND Tumor hypoxia induces vascular endothelial growth factor (VEGF) expression, which stimulates angiogenesis and tumor proliferation. The VEGF signaling pathway is inhibited by soluble VEGF receptors (soluble fetal liver kinase 1; sFlk-1), which bind VEGF and block its interaction with

[Hypoxia augments the killing effect of herpes simplex virus thymidine kinase gene expression actuated by the promoter of the vascular endothelial growth factor gene on human hepatocellular tumor cells].

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OBJECTIVE To investigate the killing effect of herpes simplex virus thymidine kinase gene expression actuated by the promoter of the vascular endothelial growth factor gene on human hepatocellular tumor cells under hypoxic condition. METHODS Recombinant adenoviral vectors, AdVEGF-tk and AdVEGF-GFP,

Hypoxia enhances the replication of oncolytic herpes simplex virus.

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Hypoxia contributes to the resistance of tumors to conventional therapies. We hypothesized that their replication in hypoxic environments like brain or oral mucosa would make oncolytic herpes simplex viruses (HSVs) such as G207 (which has undergone clinical trials) replicate to a greater extent in

Oncolytic herpes simplex virus counteracts the hypoxia-induced modulation of glioblastoma stem-like cells.

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Glioblastoma (GBM), a fatal malignant brain tumor, contains abundant hypoxic regions that provide a "niche" to promote both the maintenance and enrichment of glioblastoma stem-like cells (GSCs) and confer resistance to chemo- and radiotherapy. Since GSCs, with an ability to resist conventional

Herpes simplex virus amplicon delivery of a hypoxia-inducible angiogenic inhibitor blocks capillary formation in hepatocellular carcinoma.

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Tumor hypoxia induces vascular endothelial growth factor (VEGF) expression, which stimulates tumor angiogenesis. The VEGF pathway is inhibited by soluble VEGF receptors (soluble fetal liver kinase-1 [sFlk-1]) that bind VEGF and block its interaction with endothelial cells. Herpes simplex virus

Hypoxia Moderates γ(1)34.5-Deleted Herpes Simplex Virus Oncolytic Activity in Human Glioma Xenoline Primary Cultures.

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Hypoxia plays a critical role in the tumor microenvironment of high-grade gliomas by promoting the glioma stem cell (GSC)-like phenotype, which displays resistance to standard therapies. We tested three glioblastoma multiforme xenograft lines (xenolines) against γ(1)34.5-deleted recombinant

[Hypoxia responsive element regulated herpes simplex virus-thymidine kinase system enhances killing effect of gancyclovir on Ewing's sarcoma cell line under hypoxic condition].

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OBJECTIVE To find out a possible approach to improve the effectiveness of radiotherapy and chemotherapy for Ewing's sarcoma by constructing a eukaryotic expression vector expressing herpes simplex virus-thymidine kinase (HSV-TK) regulated by hypoxia responsive element (HRE) under hypoxia and to

Hypoxia enhances the replication of oncolytic herpes simplex virus in p53- breast cancer cells.

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Hypoxic cancer cells are refractory to conventional chemotherapy. Herpes simplex virus type-1 (HSV-1)-derived oncolytic viruses are safe for therapy since they lack the neurovirulence gene ICP34.5. Cancer cells containing high MEK activity are permissive to the HSV-1-derived oncolytic virus, R3616.

Reporter gene imaging: effects of ganciclovir treatment on nucleoside uptake, hypoxia and perfusion in a murine gene therapy tumour model that expresses herpes simplex type-1 thymidine kinase.

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Perfusion, hypoxia and nucleoside uptake during ganciclovir therapy were determined in a murine HSV-1 TK-expressing tumour model (KBALB-STK). HSV-1 TK mRNA transcription in this cell line was confirmed by RT-PCR. BALB/c mice bearing KBALB-STK tumours accumulated

A cluster of nosocomial herpes simplex virus type 1 pneumonia in a medical intensive care unit.

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We report a cluster of 3 cases of nosocomial herpes simplex virus type 1 (HSV-1) pneumonia occurring in close temporal and physical proximity during a 1-week period, which suggested a common source. HSV-1 nosocomial pneumonia occurs in immunocompetent intubated patients and presents as otherwise

Herpes simplex virus (HSV) pneumonia in a heart transplant: diagnosis and therapy.

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Organ transplants are frequently complicated by viral infections. The period of maximum immunosuppression, 1 to 6 months posttransplantation, predisposes one to intracellular pathogens. The most common intracellular viral pathogens in transplant recipients include cytomegalovirus (CMV), herpes

Quantification of the host response proteome after herpes simplex virus type 1 infection.

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Viruses employ numerous host cell metabolic functions to propagate and manage to evade the host immune system. For herpes simplex virus type 1 (HSV1), a virus that has evolved to efficiently infect humans without seriously harming the host in most cases, the virus-host interaction is specifically

Herpes simplex virus pneumonia after cardiac surgery: report of a case.

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A rare case of a 61-year-old man who developed herpes simplex virus (HSV) pneumonia after cardiac surgery is presented. He was immunocompetent before the operation and had no history of a mucocutaneous herpesvirus infection. This potentially fatal complication was successfully managed with acyclovir

Simultaneous cytomegalovirus and herpes simplex virus pneumonia.

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A 35-year-old patient who underwent renal transplant developed persistent fever, hypoxemia, and diffuse interstitial pulmonary infiltrates one month after allograft implantation. An open lung biopsy specimen demonstrated simultaneous infection with cytomegalovirus and herpes simplex virus type 1.

Hypoxia/hepatoma dual specific suicide gene expression plasmid delivery using bio-reducible polymer for hepatocellular carcinoma therapy.

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Gene therapy is suggested as a promising alternative strategy of hepatocellular carcinoma (HCC, also called hepatoma) therapy. To achieve a successful and safe gene therapy, tight regulation of gene expression is required to minimize side-effects in normal tissues. In this study, we developed a

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