The role of HCV proteins on treatment outcomes

Table 1 Amino acid substitutions associated with the resistance to different direct-acting antiviral agents

HCV protein targets	DAAs	Pattern of mutations
NS3/4A	Boceprevir	V36M/A^a, T54A/V/S^a, V55A^a, R155K/T^a, A156T/S/V^a, V158I, D168N, V/I170A/T/L, L/M175L
	Telapevir	V36G/L/M/A^a, T54A/V/S^a, S122A/G/R, R155K/T^a, A156T/S/V^a, D168A/H/T/V
	Simeprevir	V36M, F43S, Q80K ^a, S122A/R, R155T/K^a, A156T/V, D168Q/A/H/T/V/E^a, V/I170A/T/L
NS5A	Daclatasvir	M28V/A/T, Q30R/E/H, L31F/V/M^a, Q54H/N/Y, H58D, Q62R/E, A92K/T, Y93H/N/C^a
NS5A	Ledipasvir	M28T, Q30R/H, L31V, Y93H/C
NS5B	Sofosbuvir	S282T, I434M, T179A, M289L, I293L, M434T, H479P, L159F/L320F

^aAmino acid substitution represents the significant mutations that are clearly associated with reduced the response to treatment
DAAs direct-acting antiviral agents. Bolded amino acid substitutions indicate mutations frequently found to confer resistance to DAAs. Q80K for genotype 1a; D168Q for genotype 3; Y93H for genotype 1b; S282T for genotypes 1a, 1b, and 2a. Adapted from reviews [144, 145, 148, 149, 157]

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