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本帖最后由 StephenW 于 2013-1-16 20:28 编辑
回复 z3f 的帖子
7,8,9 优秀的推理.
专家的意见:
1 ADV抑制病毒水平慢于其他NAS如LMV,ETV,LDT,或TFV
2 LMV resistance increases progressively during treatment at rates of 14–32% annually, exceeding 70% after 48 months of treatment [6]. Both LMV resistance mutations (rtM204V/I and rtA181T) confer cross-resistance to LdT and other members that belong to the L-nucleoside structural group such as Emtricitabine (FTC) and Clevudine (L-FMAU) (see Table 1). The rtM204V/I substitution does not confer cross-resistance to ADV or TFV (see Table 1), but the rtA181T/V is associated with resistance to ADV [11, 22]. The rtM204V/I and the rtL180M reduce susceptibility to ETV (see Table 1) [23].
LMV耐药每年14-32%的速度在递增,超过70%的48个月后的治疗[6]。双方LMV耐药突变(rtM204V/ I和rtA181T)会议系统的交叉耐药性,恩曲他滨(FTC)和克拉夫定(L-FMAU)(见表1)的L-核苷的结构基团,如属于LDT和其他成员。 rtM204V/ I的置换不赋予交叉耐药性ADV或TFV(见表1),但与耐ADV rtA181T/ V[11,22]。 rtM204V/ I和为rtL180M减少
ETV的易感性(见表1)[23]。
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