Tong Xiao, Chase Robert, Skelton Angela, Chen Tong, Wright-Minogue Jackie, Malcolm Bruce A
Department of Virology, Schering-Plough Research Institute, 2015 Galloping Hill Road, Kenilwoth, NJ 07033, USA.
Antiviral Res. 2006 Jun;70(2):28-38. doi: 10.1016/j.antiviral.2005.12.003. Epub 2006 Jan 13.
HCV NS3 protease variants resistant to the protease inhibitor SCH 503034 were selected. Three mutations, T54A, V170A and A156S mutations conferred low to moderate levels of resistance (<20-fold). Longer exposure (>10 passages) or selection with higher levels of compound led to the selection of a more resistant variant, A156T (>100-fold). [Lin, C., Lin, K., Luong, Y.P., Rao, B.G., Wei, Y.Y., Brennan, D.L., Fulghum, J.R., Hsiao, H.M., Ma, S., Maxwell, J.P., Cottrell, K.M., Perni, R.B., Gates, C.A., Kwong, A.D., 2004. In vitro resistance studies of hepatitis C virus serine protease inhibitors, VX-950 and BILN 2061: structural analysis indicates different resistance mechanisms. J. Biol. Chem. 279(17), 17508-17514; Lu, L., Pilot-Matias, T.J., Stewart, K.D., Randolph, J.T., Pithawalla, R., He, W., Huang, P.P., Klein, L.L., Mo, H., Molla, A., 2004. Mutations conferring resistance to a potent hepatitis C virus serine protease inhibitor in vitro. Antimicrob. Agents Chemother. 48(6), 2260-2266.] Combination with IFN-alpha drastically reduced the number of emergent colonies. Resistant colonies showed no change in sensitivity to IFN-alpha. Although the A156T mutation conferred the highest level of resistance to SCH 503034, it significantly reduced the colony formation efficiency (CFE) of the mutant replicon RNA, and rendered replicon cells less fit than those bearing wild-type replicons. Replicon cells bearing mutation A156S were less fit than wild-type in co-culture growth competition assays but showed no impact on CFE. The V170A mutation, on the other hand, did not affect replicon fitness in either assay, which was consistent with its emergence as the dominant mutant after 12 months of continuous selection. The reduced fitness of the most resistant variant suggests that it may be rare in naïve patients and that development of high-level resistance may be slow. Combination therapy with IFN-alpha should also greatly reduce the potential emergence of resistance.
选择了对蛋白酶抑制剂SCH 503034耐药的丙型肝炎病毒(HCV)NS3蛋白酶变体。三种突变,即T54A、V170A和A156S突变,赋予了低至中等水平的耐药性(<20倍)。长时间暴露(>10代)或用更高浓度的化合物进行选择,导致选择出一种耐药性更强的变体A156T(>100倍)。[林,C.,林,K.,卢昂,Y.P.,饶,B.G.,魏,Y.Y.,布伦南,D.L.,富尔格姆,J.R.,萧,H.M.,马,S.,麦克斯韦,J.P.,科特雷尔,K.M.,佩尔尼,R.B.,盖茨,C.A.,邝,A.D.,2004年。丙型肝炎病毒丝氨酸蛋白酶抑制剂VX - 950和BILN 2061的体外耐药性研究:结构分析表明不同的耐药机制。《生物化学杂志》279(17),17508 - 17514;卢,L.,皮洛特 - 马蒂亚斯,T.J.,斯图尔特,K.D.,伦道夫,J.T.,皮塔瓦拉,R.,何,W.,黄,P.P.,克莱因,L.L.,莫,H.,莫拉,A.,2004年。体外赋予对一种强效丙型肝炎病毒丝氨酸蛋白酶抑制剂耐药性的突变。《抗菌药物化疗》48(6),2260 - 2266。]与α干扰素联合使用可大幅减少出现的菌落数量。耐药菌落对α干扰素的敏感性没有变化。虽然A156T突变赋予了对SCH 503034最高水平的耐药性,但它显著降低了突变体复制子RNA的菌落形成效率(CFE),并使复制子细胞的适应性低于携带野生型复制子的细胞。携带A156S突变的复制子细胞在共培养生长竞争试验中的适应性低于野生型,但对CFE没有影响。另一方面,V170A突变在两种试验中均未影响复制子的适应性,这与其在连续选择12个月后成为优势突变体一致。耐药性最强的变体适应性降低表明它在未感染过的患者中可能很少见,并且高水平耐药性的发展可能较慢。与α干扰素联合治疗也应能大大降低耐药性出现的可能性。