The effect of the first-generation HCV-protease inhibitors boceprevir and telaprevir and the relation to baseline NS3 resistance mutations in genotype 1: experience from a small Swedish cohort

Figures & data

Table 1. Baseline RASs in the SVR-group and the non-SVR-group.

	Patient	Genotype	Subtype	RAS	Natural prevalence	Mean fold change in resistance compared to wild-type replicon
The SVR group	7	1	a
	8	1	a
	11	1	a	T54S	0.4%–3.1%	2.0–20.0
	15	1	a
	16	1	a
	18	1	a	T54S	0.4%–3.1%	2.0–20.0
	20	1	a	Q80K^a	4.8%–75.0%^a	NA^a
	26	1	a	Q80K^a	4.8%–75.0%^a	NA^a
	27	1	a	D168G^a	NO^a	2.0–20.0^a
	29	1	a
	30	1	a
	35	1	a	T55A	2.8%	2.0–20.0
	9	1	b
	19	1	b
	25	1	b
	31	1	b
	32	1	b
	34	1	b
	17	1	Missing
	22	1	Missing
The non-SVR group	2	1	a
	3	1	a
	4	1	a
	5	1	a
	6	1	a
	10	1	a
	13	1	a	T54S	0.4%–3.1%	2.0–20.0
	14	1	a
	23	1	a
	24	1	a
	28	1	a
	33	1	a
	36	1	a
	1	1	a
	12	1	b
	21	1	b

^a Q80K and D168G are not representative RASs for BOC or TVR.

Table 2. Emerging representative RASs during and after treatment with BOC or TVR, mainly V36S and R155K, in 57.1% of the non-responders.

Patient	Genotype	Subtype	RAS	Natural prevalence	Mean fold change in resistance compared to wild-type replicon	Treatment response
2	1	a	R155K	0.2%–0.9%	2–100	VB
3	1	a	Negative			VB
4	1	a	V36M, R155K	0.2%–0.6%; 0.2%–0.9%	2–20; 2–100	VB
5	1	a	V36M, R155K	0.2%–0.6%; 0.2%–0.9%	2–20; 2–100	VB
6	1	a	V36M, R155K	0.2%–0.6%; 0.2%–0.9%	2–20; 2–100	VB
10	1	a	T54S, R155K	0.4%–3.1%; 0.2%–0.9%	2–20; 2–100	VR
13	1	a	54S	0.4%–3.1%	2.0–20.0	VR
14	1	a	V36M	0.2%–0.6%	2.0–20.0	VR
23	1	a	Negative			VR
24	1	a	R155K	0.2%–0.9%	2–100	VB
28	1	a	Negative			VB
33	1	a	V36M, R155K	0.2%–0.6%; 0.2%–0.9%	2–20; 2–100	VB
36	1	a	Negative			VR
1	1	a	Missing			VB
12	1	b	Negative			VR
21	1	b	ND			AM

AM: ad mortem before end point; VB: viral break-through, a positive or negative viral load nadir, followed by a higher level; VR: viral relapse, a non-detectable viral load at the end of treatment, followed by a higher level.