Development of a syngenic murine B16 cell line-derived melanoma susceptible to destruction by neuroattenuated HSV-1

Cathie G. Miller, Claude Krummenacher, Rosalyn J. Eisenberg, Gary H. Cohen, Nigel W. Fraser

Research output: Contribution to journalArticlepeer-review

56 Scopus citations

Abstract

HSV-1 ICP34.5 mutants can slow progression of preformed tumors in rodent models. However, the current models available for study are limited due to the lack of a syngenic, low-immunogenic tumor model susceptible to HSV-1. Thus we have developed a new model to determine the role of the immune response in viral-mediated tumor destruction. The human herpesvirus entry (Hve) receptors (HveA, HveB, and HveC) and a control plasmid were transfected into B78H1 murine melanoma cells. Transfection of HveA and HveC conferred sensitivity to HSV-1 to these cells. A10 (HveA), C10 (HveC), and control cells were able to form tumors reproducibly in vivo. The transfection of the receptors into B78H1 cells did not induce a detectable in vivo immunogenicity to the tumors. Finally, A10 and C10 tumor-bearing mice treated with HSV-1 1716 had significant prolongation of survival compared to mock-treated mice. These data suggest that A10 and C10 will be useful as in vivo models for studying the role of the immune response in viral-mediated tumor destruction.

Original languageEnglish (US)
Pages (from-to)160-168
Number of pages9
JournalMolecular Therapy
Volume3
Issue number2
DOIs
StatePublished - 2001

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Molecular Biology
  • Genetics
  • Pharmacology
  • Drug Discovery

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