Abstract
BackgroundThe baculovirus (BV) Autographa californica multiple nuclear polyhedrosis virus has been used in numerous protein expression systems because of its ability to infect insect cells and serves as a useful vaccination vector with several benefits, such as its low clinical risks and posttranslational modification ability. We recently reported that dendritic cells (DCs) infected with BV stimulated antitumor immunity. The recombinant BV (rBV) also strongly stimulated peptide-specific T-cells and antitumor immunity. In this study, the stimulation of an immune response against EG7-OVA tumors in mice by a recombinant baculovirus-based combination vaccine expressing fragment C-ovalbumin (FrC-OVA-BV; rBV) was evaluated.ResultsWe constructed an rBV expressing fragment C (FrC) of tetanus toxin containing a promiscuous MHC II-binding sequence and a p30-ovalbumin (OVA) peptide that functions in the MHC I pathway. The results showed that rBV activated the CD8+ T-cell-mediated response much more efficiently than the wild-type BV (wtBV). Experiments with EG7-OVA tumor mouse models showed that rBV significantly decreased tumor volume and increased survival compared with those in the wild-type BV or FrC-OVA DNA vaccine groups. In addition, a significant antitumor effect of classic prophylactic or therapeutic vaccinations was observed for rBV against EG7-OVA-induced tumors compared with that in the controls.ConclusionOur findings showed that FrC-OVA-BV (rBV) induced antitumor immunity, paving the way for its use in BV immunotherapy against malignancies.
Highlights
The baculovirus (BV) Autographa californica multiple nuclear polyhedrosis virus has been used in numerous protein expression systems because of its ability to infect insect cells and serves as a useful vaccination vector with several benefits, such as its low clinical risks and posttranslational modification ability
We previously demonstrated that the wild-type BV Autographa californica multiple nuclear polyhedrosis virus (AcMNPV) or BV-infected dendritic cells (DCs) exert natural killer (NK) and CD8+ T cell-dependent antimetastatic effects on mice, but they are CD4+ T cell independent [4,5,6,7]
In the rBVimmunized spleen cells treated with the control peptide HIV-1 Gag, the level of OVA-specific IFN-γ was decreased to that observed in the wild-type BV (wtBV) control
Summary
The baculovirus (BV) Autographa californica multiple nuclear polyhedrosis virus has been used in numerous protein expression systems because of its ability to infect insect cells and serves as a useful vaccination vector with several benefits, such as its low clinical risks and posttranslational modification ability. The stimulation of an immune response against EG7-OVA tumors in mice by a recombinant baculovirus-based combination vaccine expressing fragment C-ovalbumin (FrC-OVA-BV; rBV) was evaluated. We previously demonstrated that the wild-type (wt) BV Autographa californica multiple nuclear polyhedrosis virus (AcMNPV) or BV-infected dendritic cells (DCs) exert natural killer (NK) and CD8+ T cell-dependent antimetastatic effects on mice, but they are CD4+ T cell independent [4,5,6,7]. These antimetastatic effects involve BV directly activating NK cells. In the present study, an rBV-based combination vaccine was developed that expressed fragment C (FrC) of tetanus toxin containing a promiscuous MHC II-binding sequence [17] and a p30-OVA peptide that functions in the MHC I pathway [18], and its potential as an antitumor vaccine was evaluated
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