ATA dose-dependently reduced the number of pfu (Figure 1b).
The EC50 of ATA, as measured using the plaque reduction
assay, was 2.9 mM. The CC50 (cytotoxic concentration at which
50% of cell viability was inhibited) of ATA in Vero cells was
211 mM as determined by MTS assay (data not shown).27 Therefore,
the selective index (SI¼CC50/EC50) of ATA ranged from .3
to .75 based on different assays.28
The effect of ATA on the yields of viral progeny in
EV71-infected cells was also assessed. In this experiment, Vero
cells were infected with EV71 (TW/2231/98) at an moi of 10
accompanied by treatment with ATA at various concentrations.
At 12 hpi, viral progeny present in cell culture media and cell
lysates were harvested, pooled and then analysed for viral
titres using a plaque assay. As shown in Figure 1(c), ATA treatment
substantially reduced the titres of EV71 viral progeny produced
in infected cells. When cells were treated with ATA at
16 mM, a decrease in viral yield of .60% was evident. The
declines in viral yields were 97% and 99% when ATA was
applied to treat the virus-infected cells at 64 and 250 mM,
respectively. These results showed that ATA could effectively
reduce the production of viral progeny in EV71-infected cells.
Different EC50 values in different assays were noted, and this
may be due to the fact that different infection conditions, such
as the moi, were employed in different assays.