Studies on Antiviral Immunity-Assisted Cancer Immunotherapy

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We attempted to examine whether or not antiviral cytotoxic T lymphocytes (CTL)-induced cytolysis of tumor cells expressing viral CTL epitope could enhance antitumor immunity in an experimental model. We used B16 murine melanoma derived from C57BL/6 (B6) mouse and murine coronavirus infection in our model. Groups of B6 mice were immunized with murine coronavirus, strain JHM (JHMV). Four weeks later, they were injected subcataneously with 2*10^6 melanoma cells. Two weeks later, infectious JHMV,JHMV-derived antigenic peptides or PBS was injected into the tumors in each group. However, there was no difference in the survival time of mice. In the second experiment, B6 mice immunized with JHMV or naive ones were vaccinated twice with irradiated B16 melanoma cells either infected with JHMV,pulsed with JHMV-derived antigenic peptides or incubated in PBS (control). Then, they were challenged with the same tumor intravenously and monitored their survival. The survival time of naive mice receirved with irradiated B16 melanoma cells infected with JHMV was significantly longer than that of control mice, although the same anticancer vaccine did not elongate the survival time of JHMV-immunized mice. JHMV-immunized mice received with irradiated B16 melanoma cells pulsed with viral peptide died as quickly as control mice. These results suggest that anti-B16 melanoma immune response is not augmented by anti-JHMV CTL response in B6 mice. However, it is necessary to test further with other tumors.