1. Resistance to Direct Acting Antiviral Therapy

2. Resistance to HCV DAAs: What is the threat level?

3. HCV Biology is the basis for resistance

4. HCV biology is the basis for cure

5. Frequency of Protease Resistance Mutations Prior to Therapy

6. Emergence of Pre-existing Resistant Variants During Treatment with DAA

7. Resistance Develops Rapidly During telaprevir monotherapy with Protease Inhibitor

8. Barrier to resistance: Combination of DAAs with different mechanism of action

9. Multiple drugs target WT and resistant virus to prevent selection of resistant variants

10. Inhibitors of NS3/4A Protease

11. SVR with PegIFN/RBV + PI requires adequate IFN response to prevent resistance

12. REALIZE: Resistance rates are higher in persons less responsive to PegIFN/RBV

13. Frequency of RAVs detected in Non-SVR Patients; Poor Interferon Responders and Interferon Responders

14. Barrier to resistance: Role of viral characteristics Telaprevir Resistance in patients who failed to achieve SVR: Subtype 1a versus 1b

15. Barrier to resistance: Role of pharmacology Clonal sequence analysis from subjects dosed with ABT-450 for 3 days

16. Barrier to resistance: Combination therapy

17. Inhibitors of NS5A Replicase Protein

18. Daclatasvir: Emergence of resistance with 14 day monotherapy

19. Potent antiviral activity of GS-5885 3-day monotherapy

20. Daclatasvir + Asunaprevir ± PegIFN/RBV in Previous PegIFN/RBV Null Responders

21. Inhibitors of NS5B polymersase: non-nucleoside inhibitors (NNIs)

22. Polymerase mutations in 89 treatment naïve HCV genotype 1 infected patients

23. PI (GS-9256) + NNI (Tegobuvir) with or without RBV for HCV genotype 1

25. Inhibitors of NS5B polymersase: nucleoside inhibitors (NIs)

26. Resistance to nucleos(t)ide inhibitors

27. Antiviral Activity of PSI-7977 alone or in combination with PSI-938

28. ELECTRON: SVR following GS-7977 ± RBV ± PegIFN x 12 weeks

29. INFORM-1: Combination of NI + PI may prevent emergence of PI resistant variants

30. Cyclophilin Antagonists: Target the host

31. Clinical implications of pre-existing mutations to DAAs – spontaneous or selected

32. SVR Rates By Treatment Week 4 Response Among Patients With or Without Baseline RAVs Detected

33. Most Common RAVs†: Detectability Declines During Follow-Up

34. ADVANCE Loss of Resistance by NS3 Position

35. EXTEND Study: Long-term Follow-up of Patients Treated with Telaprevir

36. EXTEND study: Follow-up of TLV treated patients

37. C-219: Retreatment of 9 patients after TVR monotherapy with resistance

38. Clinical implications of selection resistance to first generation HCV PIs

39. Resistance to Direct Acting Antiviral Therapy