Recombinant vesicular stomatitis viruses from DNA.

Lawson, Nathan D.; Stillman, Elizabeth A.; Whitt, Michael A.; Rose, John K.

doi:10.1073/pnas.92.10.4477

Cited by 578 publications

(548 citation statements)

References 29 publications

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“…23 Recombinant VSV(M51R)-LacZ virus was generated using the established method of reverse genetics. 24,25 After successful recovery, vaccinia virus was completely eliminated by double plaque purification, and the titers (PFU/ml) of viral stocks were determined by standard plaque assays on BHK-21 cells as described previously. 26 …”

Section: Constructs and Virus Generationmentioning

confidence: 99%

“…The development of a ''reverse genetics'' system for negative-sense RNA viruses has made it possible to engineer the genome of VSV for the construction of novel gene therapy vectors. 24,25 Recombinant VSVs expressing the herpes simplex virus thymidine kinase or the cytosine deaminase suicide genes have been reported by Barber's group. 32,33 Their results suggest that the use of the prodrug-suicide gene strategy may add synergy to the effectiveness of oncolytic VSV in cancer treatment.…”

Section: Mutant Vsv For Treatment Of Breast Cancer O Ebert Et Almentioning

confidence: 99%

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Systemic therapy of experimental breast cancer metastases by mutant vesicular stomatitis virus in immune-competent mice

et al. 2004

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In view of the limited success of available treatment modalities for metastatic breast cancer, alternative and complementary strategies need to be developed. Oncolytic vesicular stomatitis virus (VSV) is a promising novel therapeutic agent for the treatment of cancer. The aim of this study was to evaluate the potential of recombinant VSV containing the M51R mutation in the matrix (M) protein gene administered intravenously as an effective and safe therapeutic agent for treating mice with experimental breast cancer metastases. Recombinant VSV(M51R)-LacZ was generated and characterized in vitro on human and murine breast cancer cells. Breast cancer metastases were established in immune-competent Balb/c mice by intravenous injection of syngeneic 4T1 cells. The vector was infused into the tumor-bearing animals via the tail vein, and productive infection of pulmonary breast cancer lesions was assessed by X-gal stainings of frozen lung sections. To evaluate potential systemic toxicity, histology of major organs and serum chemistries were analyzed. To assess effectiveness, buffer-or vector-treated tumor-bearing mice were followed for survival and the results were analyzed by the Kaplan-Meier method and the log-rank test. We found that VSV(M51R)-LacZ efficiently replicated and lysed human breast cancer cells but was partially attenuated in 4T1 cells in vitro. We also demonstrated that its maximum tolerated dose after intravenous infusion in normal Balb/c mice was elevated by at least 100-fold over that of the parental VSV vector containing the wild-type M gene. When VSV(M51R)-LacZ was repeatedly injected intravenously into mice bearing syngeneic 4T1 tumors, the virus was able to infect multiple breast cancer lesions in the lungs without apparent toxicities, which led to significant prolongation of animal survival (P ¼ .003). In conclusion, systemic administration of M mutant VSV is both effective and safe in the treatment of experimental breast cancer metastases in immune-competent mice, suggesting that further development of this approach may have potential for clinical application in patients.

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Section: Constructs and Virus Generationmentioning

confidence: 99%

Section: Mutant Vsv For Treatment Of Breast Cancer O Ebert Et Almentioning

confidence: 99%

Systemic therapy of experimental breast cancer metastases by mutant vesicular stomatitis virus in immune-competent mice

et al. 2004

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“…13 VSV represents an excellent choice as a vector for suicide gene transduction because of selective cancer cell tropism and the relative ease of foreign gene insertion. 4,5,14 VSV engineered to express suicide enzymes allow the conversion of non-toxic prodrug into a toxic form only at the site of viral replication, thus generating specific bystander killing at the tumor site. Recombinant VSV carrying the Herpes virus TK enzyme has been shown to phosphorylate the non-toxic prodrug ganciclovir, facilitating its DNA integration and subsequent local toxicity.…”

Section: Introductionmentioning

confidence: 99%

Enhancing VSV oncolytic activity with an improved cytosine deaminase suicide gene strategy

Léveillé

Samuel

et al. 2011

Cancer Gene Ther

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Oncolytic viruses (OVs) are promising therapeutic agents for cancer treatment, with recent studies emphasizing the combined use of chemotherapeutic compounds and prodrug suicide gene strategies to improve OV efficacy. In the present study, the synergistic activity of recombinant vesicular stomatitis virus (VSV)-MD51 virus expressing the cytosine deaminase/uracil phosphoribosyltransferase (CD::UPRT) suicide gene and 5-fluorocytosine (5FC) prodrug was investigated in triggering tumor cell oncolysis. In a panel of VSV-sensitive and -resistant cells-prostate PC3, breast MCF7 and TSA, B-lymphoma Karpas and melanoma B16-F10-the combination treatment increased killing of non-infected bystander cells in vitro via the release of 5FC toxic derivatives. In addition, we showed a synergistic effect on cancer cell killing with VSV-MD51 and the active form of the drug 5-fluorouracil. Furthermore, by monitoring VSV replication at the tumor site and maximizing 5FC bioavailability, we optimized the treatment regimen and improved survival of animals bearing TSA mammary adenocarcinoma. Altogether, this study emphasizes the potency of the VSV-CD::UPRT and 5FC combination, and demonstrates the necessity of optimizing each step of a multicomponent therapy to design efficient treatment.

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“…The recovery of infectious viruses from cloned and transfected cDNA will be an innovative technology, enabling the genetic engineering of viruses in this superfamily. The DNA transfection system has been established for two rhabdoviruses: rabies virus (Schnell et al 1994) and vesicular stomatitis virus (VSV) (Lawson et al 1995;Whelan et al 1995), with a genome of about 12 kilobases (kb), and for three paramyxoviruses: measles (Radecke et al 1995), Sendai (Garcin et al 1995), and RS (Collins et al 1995) viruses, with an approximate 15 kb genome. These systems, except for that of the measles virus, employed the transfection of cDNA into cells in which the cDNA and the plasmids carrying the viral nucleocapsid protein (NP or N) and RNA polymerase genes are coexpressed by vaccinia virus (VV)-driven bacteriophage T7 RNA polymerase (T7 pol).…”

Section: Introductionmentioning

confidence: 99%

Initiation of Sendai virus multiplication from transfected cDNA or RNA with negative or positive sense

et al. 1996

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Background: The mononegavirus superfamily (Mononegavirales) comprises three families, Rhabdoviridae, Paramyxoviridae and Filoviridae. These viruses possess a single stranded negative sense RNA as the genome. Recentsuccessintherecoveryofinfectiousvirusfroma transfected cDNA of mononegaviruses including Sendai virus, a prototypic paramyxovirus, is opening the possibility of their genetic engineering. However, infectious viruses have been recovered only by initiating the infectious cycle with cDNA directing the synthesis of antigenomic positive sense ( ) RNA. Starting with genomic negative sense (ÿ) RNA has been unsuccessful. Furthermore, the recovery efficiency has often been extremely low.

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Recombinant vesicular stomatitis viruses from DNA.

Cited by 578 publications

References 29 publications

Systemic therapy of experimental breast cancer metastases by mutant vesicular stomatitis virus in immune-competent mice

Systemic therapy of experimental breast cancer metastases by mutant vesicular stomatitis virus in immune-competent mice

Enhancing VSV oncolytic activity with an improved cytosine deaminase suicide gene strategy

Initiation of Sendai virus multiplication from transfected cDNA or RNA with negative or positive sense

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