Table 1.
Baseline characteristics.
Fig 1.
Prevalence of RASs after failure of combination therapy with daclatasvir and asunaprevir.
Prevalence of RAS in NS3 (a) and NS5A(b).
Table 2.
RAS in NS3 and NS5A regions after failure of daclatasvir/asenaprevir combination therapy.
Fig 2.
Prevalence of signature RASs in NS5A after treatment failure.
The prevalence of signature RAS at L31 and Y93 in NS5A after treatment failure in total patients.
Fig 3.
Prevalence of signature RASs in NS5A after treatment failure in terms of baseline RASs.
The prevalence of signature RAS at L31 and Y93 in NS5A after treatment failure in patients stratified by presence of baseline RASs. Even in patients without L31/Y93 RAS at baseline, dual RAS at L31 plus Y93 emerged after treatment failure. The prevalence of dual RASs was not significantly different between patients with and without RASs at baseline (p = 0.08).
Fig 4.
Prevalence of signature RASs in NS5A in terms of reasons for treatment failure.
The prevalence of signature RAS at L31 and/or Y93 in NS5A in patients who stopped the therapy by adverse events was significantly low than others.
Fig 5.
Prevalence of other RASs within NS5A in combination with signature L31/Y93 RAS.
Other RAS in combination with dual signature RAS (L31-RAS/Y93-RAS) were detected in 53% of patients. The prevalences of triple, quadruple, and quintuple RAS were 38%, 13%, and 2%, respectively.
Fig 6.
Co-existence of signature RASs in NS3 and NS5A.
The prevalence of co-existence of signature RAS in NS3 and NS5A was analyzed. The prevalence of concomitant D168 RAS with L31 and/or Y93 RAS was 62%.