The impact of Spn4A.RRLL(s) treatment on HCV replication was further investigated using HCV subgenomic replicons [75] . Human hepatoma cells harbouring stable HCV replicons encoding wild-type NS5A (Huh.8 cells) or NS5A with an adaptive mutation (Huh.2 cells) were treated with recombinant adenoviruses for 5 days. Total RNA levels were then harvested and the level of HCV RNA was quantified using QPCR analysis. No significant differences were observed between HCV replicon levels treated with Spn4A.RRLL(s), Spn4A.RRLL(r), and the control (Ad-Empty) ( Figure 5D ). These results confirm that Spn4A. RRLL(s) does not inhibit HCV replication. These findings, in addition to the measured decrease in LDLR expression presented in Figure 3B , strongly suggest that the robust reduction in intracellular HCV RNA levels observed in Spn4A.RRLL(s) pretreated cells prior to HCV infection is, at least in part, due to reduced viral attachment or entry.