TABLE 1.
Prime (dose)/route | Adjuvant | Boost (dose)/route | Adjuvant (dose) | na | P18-specific IFN-γ SFCb | P18-specific tetramer + CD8 cellsc |
---|---|---|---|---|---|---|
Peptide (50 μg)/i.n. | Cholera toxin (1 μg) | Peptide (50 μg × 3)/i.n. | Cholera toxin (1 μg) | 9 | 116.2 ± 32.9 | 2.8 ± 0.28 |
Peptide (50 μg)/i.n. | Cholera toxin (1 μg) | MVA (107 PFU)/i.d. | None | 12 | 502.3 ± 99.9d | 4.8 ± 0.53d |
Peptide (50 μg)/i.n. | Cholera toxin (1 μg) | DNA (50 μg)/i.m. | None | 4 | 19.1 ± 6.4 | 1.3 ± 0.09 |
None/i.n. | Cholera toxin (1 μg) | None/i.n. | Cholera toxin (1 μg) | 4 | 5 ± 2.0 | 0.5 ± 0.10 |
MVA (107 PFU)/i.d. with minigene | None | Peptide (50 μg)/i.n. | Cholera toxin (1 μg) | 4 | 243 ± 62.0 | 2.1 ± 0.16 |
MVA (107 PFU)/i.d. with minigene | None | MVA (107 PFU)/i.d. with minigene | None | 12 | 438.6 ± 77.6e | 8.4 ± 0.81e |
MVA (107 PFU)/i.d. with minigene | None | DNA (50 μg)/i.m. | None | 12 | 113.6 ± 21.4 | 3.1 ± 0.40 |
MVA (107 PFU)/i.d. with minigene | None | None | None | 4 | 176 ± 41.0 | 2.4 ± 0.19 |
MVA (107 PFU)/i.d. without minigene | None | MVA (107 PFU)/i.d. without minigene | None | 4 | 5 ± 2.0 | 0.5 ± 0.10 |
DNA (50 μg)/i.m. | None | Peptide (50 μg)/i.n. | Cholera toxin (1 μg) | 10 | 11.4 ± 3.8 | 0.8 ± 0.06 |
DNA (50 μg)/i.m. | None | Peptide (50 μg × 3)/i.n. | Cholera toxin (1 μg) | 12 | 103 ± 31.5 | 2.6 ± 0.18 |
DNA (50 μg)/i.m. | None | MVA (107 PFU)/i.d. with minigene | None | 12 | 380 ± 76.0f | 9.4 ± 0.96f |
DNA (50 μg)/i.m. | None | DNA (50 μg)/i.m. | None | 4 | 8.3 ± 3.1 | 1.1 ± 0.08 |
DNA (50 μg)/i.m. | None | None | None | 3 | 11.6 ± 2.6 | 0.8 ± 0.09 |
PMV plasmid (50 μg)/i.m. | None | PMV plasmid (50 μg)/i.m. | None | 4 | 6.3 ± 2.0 | 0.4 ± 0.02 |
n, number of mice.
Data are means ± standard error, per 1, million cells.
Data are means ± standard errors.
Compared to all regimens primed with peptide, peptide prime-rMVA boost induced significantly more IFN-γ SFCs and tetramer-specific cells when compared by t test (P < 0.05). Analysis by ANOVA was comparable in the IFN-γ ELISpot assay (P = 0.05), but did not reveal highly significant differences in tetramer-specific cells between peptide-rMVA and peptide-peptide three-dose regimens or peptide-rMVA and peptide-DNA.
Compared to all regimens primed with rMVA rMVA prime-rMVA boosting induced significantly more tetramer-specific cells when compared by t test (P < 0.05) and by ANOVA (P = 0.05). Analysis by ANOVA was comparable but did not reveal highly significant differences between rMVA-rMVA and rMVA-peptide or rMVA-rMVA and rMVA-no-treatment regimens by the ELISpot assay.
Compared to all regimens primed with DNA, DNA-rMVA induced significantly more IFN-γ SFCs and tetramer-specific cells when compared by t test (P < 0.05). Analysis by ANOVA was comparable in the tetramer binding assay; however, ANOVA only demonstrated highly significant results (P = 0.05) when DNA-rMVA was compared to DNA-peptide by the IFN-γ ELISpot assay.