Viral gene therapy against malignant tumors holds great promise for tumors that are susceptible to the oncolytic activity of viruses. “Extended release of an anti-heparan sulfate peptide from a contact lens suppresses corneal Herpes Simplex Virus-1 (HSV-1) infection”. Thus, the potential risks associated with the use of gene therapy in this group would appear reasonable. We are also exploring the events during primary KSHV infection, including interactions between the virus and cell membrane, modulation of host gene synthesis, and establishment of viral infection. In vitro synergy was further observed with other chemotherapeutic agents. Non-aggressive tumours were defined as well-differentiated with a Gleason score ≤6. Furthermore, we found that HHV-8 triggered epithelial-to-mesenchymal transition.
The IL-12-mediated enhancement observed with NV1042 in the syngeneic model was abrogated in athymic mice treated in a similar manner, thus indicating a role for T cells in the augmented efficacy of NV1042 virus. Our results suggest that the cav-1 promoter may have unique benefits in targeting gene therapy to prostate cancer and its associated vasculature. Using human and animal models for prostate cancer we have demonstrated that adenovirus-mediated transfer of the HSV-tk gene resulted in sensitivity to ganciclovir in vitro and growth suppression of mouse prostate cancer in vivo.