TABLE 3.
In vivo treatment | PWF
|
Serum
|
|||
---|---|---|---|---|---|
HSV-1a (log10 PFU/ml) | Antiviral activityb (mIFN-α IU/ml) | IFN-γc (101 pg/ml) | Antiviral activity (mIFN-α IU/ml) | IFN-γ (101 pg/ml) | |
NRSd + vehiclee | 1.7 ± 0.2f | 17.6 ± 6.0 | <6 ± 0 | 29.7 ± 13.4 | <30 ± 0 |
AGMh + vehicle | 1.8 ± 0.2 | 14.7 ± 5.5 | <6 ± 0 | 18.3 ± 8.5 | <30 ± 0 |
NRS + IL-18 | <0.7 ± 0.0 | <1.0 ± 0.0 | 48 ± 20g | <10.0 ± 0.0 | <30 ± 0 |
AGM + IL-18 | <0.7 ± 0.0 | <1.0 ± 0.0 | <6 ± 0 | <10.0 ± 0.0 | <52 ± 28 |
HSV-1 was titrated by plaque assay with Vero cells.
Antiviral activity was measured by using VSV and mouse L929 cells and is expressed as the mIFN-α titer.
Measured by ELISA.
NRS or anti-asialo GM1 antibody was injected i.p. on days 3 and 1 before infection.
On days 2 and 1 before infection and days 0 and 1 of infection, 1 μg of IL-18 was injected i.p. into each mouse (n = 3 per group), and the mice were sacrificed to prepare PWF and serum 2 h after the final injection with the vehicle or IL-18.
Mean ± standard deviation.
Significantly increased values compared to those of mice treated with anti-asialo GM1 antibody plus IL-18 (P < 0.01).
AGM, anti-asialo GM1 antibody.