期刊
MOLECULAR THERAPY
卷 3, 期 2, 页码 160-168出版社
ACADEMIC PRESS INC
DOI: 10.1006/mthe.2000.0240
关键词
HSV-1; tumor model; melanoma; gene therapy; Hve receptor
资金
- NCI NIH HHS [CA 77903] Funding Source: Medline
- NINDS NIH HHS [NS 07180, NS 37516] Funding Source: Medline
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.
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