Recent study studied the quercetin as a potential nontoxic anti-HCV agent in reducing viral production by inhibiting both NS3 and heat shock proteins (that are essential for HCV replication). It was found that quercetin inhibit NS3 activity in a specific dose-dependent manner in vitro catalysis assay. Moreover, as analyzed in the subgenomic HCV RNA replicon system, quercetin seemed to exert adjunctive effect: to inhibit HCV RNA replication and production in the HCV infectious cell culture system (HCVcc), as analyzed by the focusforming unit reduction assay and HCV RNA real-time PCR. The inhibitory effect of quercetin was also obtained when using a model system in which NS3-engineered substrates were introduced in NS3-expressing cells, providing evidence that inhibition in vivo could be directed to NS3 and does not involve other HCV proteins. This work demonstrates that quercetin has a direct inhibitory effect on the HCV NS3 protease [32] . (9) showed anti-HBV activity in vitro. Anti-HBV activity was closely related to the parent structure of these compounds (agigenin > luteolin > quercetin) as well as to the number of glucoside (flavone monoglucoside > flavone diglucoside). The structure of these agent also influences their cytotoxicity (flavone > flavone monoglucoside > flavone diglucoside). In addition, the substitution of acyl group on glucoside may be important to keep their anti-HBV activities (galloyl > feruloyl > coumaroyl) [33] . Quercetin did not show activities against HBeAg secretion: this limit might be due to the absence of the saccharide group in their structures [34] .