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7. Treatment of Experimental Intracranial Murine Melanoma with a Neuroattenuated Herpes Simplex Virus 1 Mutant

Author

Randazzo, Bruce P., Kesari, Santosh, Gesser, Richard M., Alsop, David, Ford, John C., Brown, S. Moira, Maclean, Alasdair, and Fraser, Nigel W.

Abstract

Brain metastases occur commonly in the setting of a variety of human cancers. At present, such cases are invariably fatal and highlight a need for research on new therapies. We have developed a mouse brain tumor model utilizing the Harding-Passey melanoma cell line injected intracranially into C57BI/6 mice. Tumors develop in 100% of the mice and can be detected by magnetic resonance imaging as early as 5 days post cell injection. Death from tumor progression occurs between 12 and 16 days post cell injection. Stereotactic injection of the neuroattenuated HSV-1 strain 1716 into brain tumors 5 or 10 days postinjection of the melanoma cells results in a statistically significant increase in the time to development of neurological symptoms and in complete tumor regression and the long-term survival of some treated animals. Moreover, viral titration studies and immunohistochemistry suggest that replication of this virus is restricted to tumor cells and does not occur in the surrounding brain tissue. These results suggest that HSV-1 mutant 1716 shows particular promise for use as a therapeutic agent for the treatment of brain tumors. Copyright 1995, 1999 Academic Press

Published
1995
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8. Genetic studies with herpes simplex virus type 1

Author

Brown, S. Moira and Brown, S. Moira

Abstract

The work presented in this thesis was concerned with the genetical analysis of Herpes simplex virus Type 1 (Glasgow strain 17). The study involved the use of two types of mutant:- (1) Conditional lethal mutants of the temperature sensitive (ts) type which are able to grow at 31

9. Antitumor activity of a selectively replication competent herpes simplex virus (HSV) with enzyme prodrug therapy.

Author

Braidwood L, Dunn PD, Hardy S, Evans TR, and Brown SM

Subjects
Animals, Blotting, Western, Combined Modality Therapy, Female, Herpes Simplex genetics, Herpes Simplex pathology, Herpes Simplex virology, Herpesvirus 1, Human genetics, Humans, Immunoenzyme Techniques, Mice, Mice, Nude, Neoplasms, Experimental genetics, Neoplasms, Experimental virology, Oncolytic Viruses genetics, Polymerase Chain Reaction, Prodrugs pharmacokinetics, Tissue Distribution, Virus Replication, Antineoplastic Agents therapeutic use, Aziridines therapeutic use, Herpesvirus 1, Human pathogenicity, Neoplasms, Experimental therapy, Oncolytic Viruses metabolism, Prodrugs therapeutic use
Abstract

Background: HSV1790 is an oncolytic virus generated by inserting the enzyme nitroreductase (NTR) into the virus HSV1716. NTR converts the prodrug CB1954 into an active alkylating agent., Materials and Methods: In vitro, 3T6 cells (non permissive to HSV) were used in order to distinguish between virus-induced cytopathic effect and cell death due to activated prodrug. In vivo, xenograft models were injected with HSV1790 (10(5)-10(9) PFU) with or without CB1954 (max 80mg/kg) and tumor volume recorded regularly. Biodistribution of HSV1790 was determined immunohistochemically and by PCR., Results: HSV1790 + CB1954 in vitro was more effective at killing tumor cells than the virus or the prodrug alone. In vivo, the combination reduced tumor volume and increased survival compared to treatment with HSV1790 or CB1954 alone. Following systemic administration of HSV1790, viral replication was detected in tumors, but not organs., Conclusion: HSV1790 + prodrug enhances tumor cell killing in vitro and reduces tumor volume and increases survival in vivo.

Published
2009

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