Science Advances

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• Materials and Methods
• Fig. S1. Structural illustration of a G-quartet.
• Fig. S2. Conservation analysis of HCV genomes.
• Fig. S3. Premade sequence alignment in the central part of the HCV C gene, between positions +253 and +294.
• Fig. S4. Premade sequence alignment in the central part of the HCV C gene, between positions +253 and +294.
• Fig. S5. Premade sequence alignment in the central part of the HCV C gene, between positions +253 and +294.
• Fig. S6. Expansion of the ¹H NMR spectra of RNA1a.
• Fig. S7. Expansion of the ¹H NMR spectra of RNA1b.
• Fig. S8. Prediction of the RNA secondary structure of the C gene (subtype 1a) using free-energy minimization.
• Fig. S9. Prediction of the RNA secondary structure of the C gene (subtype 1b) using free-energy minimization.
• Fig. S10. G4 formation in a long structural context evidenced by ¹H NMR.
• Fig. S11. Synthetic HCV G-rich sequences form parallel G4 RNAs.
  
• Fig. S12. G4 structure of RNA1a is more stable than that of RNA1b.
  
• Fig. S13. G4 RNAs are characterized in the presence of alkali metal ions (K⁺, Na⁺, or Li⁺).
  
• Fig. S14. HCV G4 RNA structures are destabilized through the ASO.
  
• Fig. S15. CD melting curves of HCV G-rich RNAs.
  
• Fig. S16. Influence of different alkali metal ions on the thermal stabilities of HCV G4 RNAs.
• Fig. S17. Analysis of concentration-independent melting curves of target HCV RNAs.
  
• Fig. S18. CD melting studies of target HCV RNAs.
  
• Fig. S19. Structures of TMPyP4 and TMPyP2.
  
• Fig. S20. G4 ligand stabilizes target HCV G4 RNAs.
  
• Fig. S21. Little interaction is observed between the G4 ligand and G4-mutated RNAs.
  
• Fig. S22. Schematic depiction of the inhibition of FRET through the binding between PDP and G4 RNA.
  
• Fig. S23. PDP binds to target G4 RNA and inhibits the trap by the corresponding ASO.
  
• Fig. S24. G4 ligand inhibits RNA-dependent RNA synthesis through G4 RNA stabilization.
  
• Fig. S25. Map of the plasmid 24480 (pMO29) and a sequenced portion of this plasmid for verification.
  
• Fig. S26. TMPyP2 does not stabilize G4 RNA for RNA1b.
  
• Fig. S27. G4 ligands do not suppress the expression of the HCV C gene containing a G4-mutated sequence.
  
• Fig. S28. G4 ligands repress the in vitro expression of EGFP through G4 RNA stabilization.
  
• Fig. S29. G4 ligands do not repress the in vitro expression of EGFP in empty vector or G4-mutated plasmids.
• Fig. S30. Sequence of the C gene for HCV JFH1 virus.
  
• Fig. S31. Premade sequence alignment in the central part of the HCV C gene (subtype 2a), between positions +253 and +296.
  
• Fig. S32. Premade sequence alignment in the central part of the HCV C gene (subtype 2a), between positions +253 and +296.
  
• Fig. S33. Premade sequence alignment in the central part of the HCV C gene (subtype 2a), between positions +253 and +296.
  
• Fig. S34. Graphical representation of G-rich consensus sequences in genotype 2a HCV genomes.
  
• Fig. S35. G4 RNA structure of RNA2a evidenced in different studies.
  
• Fig. S36. G4 ligands inhibit intracellular HCV JFH1 replication.
  
• Fig. S37. Sequence of the C gene for HCV H77.
  
• Fig. S38. Sequence of the C gene for HCV Con1.
  
• Fig. S39. G4 ligands suppress intracellular HCV H77/JFH1 replication.
  
• Fig. S40. Western blot analysis shows suppression of intracellular HCV H77/JFH1 replication through G4 ligands.
  
• Fig. S41. Detection of HCV⁻ RNA using Tth-based RT-qPCR.
  
• Fig. S42. Structure of biotin-PDP.
  
• Fig. S43. Biotin modification on PDP does not impair the stabilization of HCV G4 RNAs.
  
• Fig. S44. Pull down of G4 RNA through biotin-PDP.
  
• Fig. S45. HCV G4 RNAs evidenced by a selective G4 affinity probe.
  
• Fig. S46. G4 ligands do not inhibit influenza A virus without a G-rich region.
  
• Fig. S47. ASOs destabilize the HCV G4s and show stimulatory effects on viral replication.
  
• Fig. S48. Target HCV sequences form intracellular G4 structures.
  
• Fig. S49. Target HCV sequences form intracellular G4 structures probed by the G4 ligand.
  
• Fig. S50. G4 ligand binds to the target G4 site in the full HCV genome under physiological conditions.
  
• Table S1. GenBank accession numbers of the HCV genomes analyzed.
  
• Table S2. List of 1056 sequenced partial cds of the C genes for subtype 1a.
  
• Table S3. List of 1025 sequenced partial cds of the C genes for subtype 1b.
  
• Table S4. Sequences of oligomers used in our studies.
  
• Table S5. Calculated T_m of synthetic HCV G-rich sequences in the presence of different alkali metal ions.
  
• Table S6. List of 143 sequenced partial cds of the C genes for subtype 2a.

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