Figure 3
Figure 3. In situ FX zymogen activation or combining thrombin/FXa/FVIIa enhances HSV1 infection. HUVECs in SFM were inoculated with the indicated type of HSV1 (4.5 × 105 vp/mL) in the absence (open symbols) or presence (closed symbols) of FVIIa (0.5nM) and varied FX or 20nM FX (A; n = 3; data are ± SEM) or a mixture of thrombin (100nM)/FXa (10nM)/FVIIa (5nM) at various dilutions (B; n = 4; data are ± SEM). The number of plaques was determined 24 hours after infection. The data were corrected for the number of plaques detected in the presence of FVIIa alone (0.5nM) or added protease mix, respectively.

In situ FX zymogen activation or combining thrombin/FXa/FVIIa enhances HSV1 infection. HUVECs in SFM were inoculated with the indicated type of HSV1 (4.5 × 105 vp/mL) in the absence (open symbols) or presence (closed symbols) of FVIIa (0.5nM) and varied FX or 20nM FX (A; n = 3; data are ± SEM) or a mixture of thrombin (100nM)/FXa (10nM)/FVIIa (5nM) at various dilutions (B; n = 4; data are ± SEM). The number of plaques was determined 24 hours after infection. The data were corrected for the number of plaques detected in the presence of FVIIa alone (0.5nM) or added protease mix, respectively.

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