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. 2004 Dec;78(23):13163–13172. doi: 10.1128/JVI.78.23.13163-13172.2004

TABLE 1.

Immunization regimens

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
a

n, number of mice.

b

Data are means ± standard error, per 1, million cells.

c

Data are means ± standard errors.

d

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.

e

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.

f

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.