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Table 2 Amino acid substitutions in 18 NS3 positions of interest

From: A 3-year follow-up study after treatment with simeprevir in combination with pegylated interferon-α and ribavirin for chronic hepatitis C virus infection

NS3 amino acid profile at time of failurea

N

Return to baseline at EOSa,c,d, n (%)

Change to new profile at EOSa,c, n (%)

Follow-up timeb, median, weeks

Follow-up timeb, range, weeks

All HCV geno/subtypes

Enrolled patients with no SVR at LPVPS

49

    

 Number of patients (at failure with EOS) with sequencing informationc

48

37 (77.1)

3 (6.3)

177.7

(46.7–230.3)

  No emerging NS3 amino acid substitution

5

0 (0.0)

0 (0.0)

174.0

(111.3–192.0)

  Any emerging NS3 amino acid substitution

43

37 (86.0)

3 (7.0)

179.9

(46.7–230.3)

HCV GT1a with Q80K at baseline

Enrolled patients with no SVR at LPVPS

10

    

 Number of patients (at failure with EOS) with sequencing informationc

10

8 (80.0)

0 (0.0)

146.9

(96.1–230.3)

  No emerging NS3 amino acid substitution

1

0 (0.0)

0 (0.0)

111.3

–

  Any emerging NS3 amino acid substitution

9

8 (88.9)

0 (0.0)

180.9

(96.1–230.3)

   R155K

8

8 (100.0)

0 (0.0)

146.9

(96.1–230.3)

   D168E

1

0 (0.0)

0 (0.0)

192.4

–

HCV GT1a without Q80K at baseline

Enrolled patients with no SVR at LPVPS

14

    

 Number of patients (at failure with EOS) with sequencing informationc

14

12 (85.7)

1 (7.1)

182.6

(98.9–222.0)

  Any emerging NS3 amino acid substitution

14

12 (85.7)

1 (7.1)

182.6

(98.9–222.0)

   R155K

4

3 (75.0)

0 (0.0)

179.4

(98.9–198.0)

   D168V

2

2 (100.0)

0 (0.0)

141.6

(138.0–145.1)

   Q80R + D168E

2

2 (100.0)

0 (0.0)

214.4

(210.0–218.7)

   R155K + D168E

2

1 (50.0)

1 (50.0)

182.6

(182.1–183.0)

   D168A

1

1 (100.0)

0 (0.0)

134.6

–

   D168E

1

1 (100.0)

0 (0.0)

192.0

–

   R155K + D168A

1

1 (100.0)

0 (0.0)

189.0

–

   R155K + D168V

1

1 (100.0)

0 (0.0)

222.0

–

HCV GT1b

Enrolled patients with no SVR at LPVPS

24

    

 Number of patients (at failure with EOS) with sequencing informationc

24

17 (70.8)

2 (8.3)

174.9

(46.7–225.1)

  No emerging NS3 amino acid substitution

4

0 (0.0)

0 (0.0)

175.3

(157.1–192.0)

  Any emerging NS3 amino acid substitution

20

17 (85.0)

2 (10.0)

174.9

(46.7–225.1)

   D168V

10

10 (100.0)

0 (0.0)

148.5

(46.7–225.1)

   Q80R + D168E

2

0 (0.0)

1 (50.0)

169.5

(126.9–212.1)

   D168A

1

1 (100.0)

0 (0.0)

188.4

–

   D168E

1

1 (100.0)

0 (0.0)

169.3

–

   D168E/V

1

1 (100.0)

0 (0.0)

220.3

–

   Q80K + D168E

1

1 (100.0)

0 (0.0)

174.6

–

   Q80K + S122R + D168E

1

0 (0.0)

1 (100.0)

175.9

–

   Q80R + D168E/V

1

1 (100.0)

0 (0.0)

196.3

–

   Q80R + S174F/Y

1

1 (100.0)

0 (0.0)

166.4

–

   V132I + D168V

1

1 (100.0)

0 (0.0)

221.0

–

  1. The above table presents return-to-baselinea,c,d or change to newa,c amino acid substitution in 18 NS3 positions of interesta at the end of this follow-up study, by HCV genotype/subtype and presence of baseline NS3 Q80K, in patients with no SVR at LPVPS
  2. EOS end of study, GT genotype, HCV hepatitis C virus, LPVPS last post-therapy follow-up visit of the parent study, SVR sustained virologic response
  3. aOnly emerging NS3 amino acid substitutions at 18 selected positions (36, 41, 43, 54, 55, 80, 107, 122, 132, 138, 155, 156, 158, 168, 169, 170, 174,175) were considered
  4. bFollow-up time is the time (weeks) between the date of the last available sample in this study and the time of failure sample from the parent study
  5. cEOS: last available sequencing sample from this study
  6. dReturn to baseline: return to amino acid substitutions that were present at baseline, or to wildtype
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