Biology Reference
In-Depth Information
Figure 2.
Viral DNA yield obtained at 24 hr post-infection. Left panel: Electropherogram of the
de
novo
synthesized progeny viral DNA (form I) indicated by the arrow. Lane 1: Mock infected cells,
Lane 2: Untreated control cells; Lane 3, and 4: Cells treated with RV 20 μM and 40, respectively.
Right panel: Quantification of the fluorescence bands reported in the left panel. The yield of the viral
DNA is normalized to the amount obtained in untreated control cells (Bar 1). Bar 3 and bar 4: viral
DNA obtained after treatment with RV 20 μM and 40, respectively.
To assess whether the continuous presence of RV is necessary to inhibit the viral
replication we removed the drug at different time points after the viral penetration
into the cell (Figure 3). Therefore, the infection was carried out in 20 μM RV but the
culture medium was changed to a drug-free fresh medium after different times of treat-
ment and the incubation was continued for 24 hr. Results show that removal of RV
after 4 hr incubation has little or no effect on the yield of viral progeny DNA (Lane 2).
The drug must be present for the whole infection time to be effective and to cause the
complete inhibition of the viral replication (Lanes 6 and 7).
Figure 3.
Decrease of viral DNA as a function of the duration of the exposure to resveratrol. Left panel:
Progeny viral DNA (form I) is indicated by the arrow. In this case, the culture medium was changed
to fresh drug-free medium at the following times post-infection. The incubation was continued for
24 hr. Lane 1: Mock infected cells; Lane 2: Untreated control cells; Lane 3 through 6: 4, 8, 12, and
16 hr, respectively; Lane 7: The medium was not changed and infection was carried permanently in
the presence of RV (20 μM). Right panel: Quantification of the fluorescence bands reported in the
left panel. The yield of the viral DNA is normalized to the amount obtained in untreated control cells
(Bar 1). Withdrawal of RV is reported in the legend to left panel of this figure.
