Tenney Daniel J, Rose Ronald E, Baldick Carl J, Levine Steven M, Pokornowski Kevin A, Walsh Ann W, Fang Jie, Yu Cheng-Fang, Zhang Sharon, Mazzucco Charles E, Eggers Betsy, Hsu Mayla, Plym Mary Jane, Poundstone Patricia, Yang Joanna, Colonno Richard J
Bristol-Myers Squibb Pharmaceutical Research Institute, 5 Research Parkway, Wallingford, CT 06492, USA.
Antimicrob Agents Chemother. 2007 Mar;51(3):902-11. doi: 10.1128/AAC.00833-06. Epub 2006 Dec 18.
Entecavir (ETV) is a deoxyguanosine analog approved for use for the treatment of chronic infection with wild-type and lamivudine-resistant (LVDr) hepatitis B virus (HBV). In LVD-refractory patients, 1.0 mg ETV suppressed HBV DNA levels to below the level of detection by PCR (<300 copies/ml) in 21% and 34% of patients by Weeks 48 and 96, respectively. Prior studies showed that virologic rebound due to ETV resistance (ETVr) required preexisting LVDr HBV reverse transcriptase substitutions M204V and L180M plus additional changes at T184, S202, or M250. To monitor for resistance, available isolates from 192 ETV-treated patients were sequenced, with phenotyping performed for all isolates with all emerging substitutions, in addition to isolates from all patients experiencing virologic rebounds. The T184, S202, or M250 substitution was found in LVDr HBV at baseline in 6% of patients and emerged in isolates from another 11/187 (6%) and 12/151 (8%) ETV-treated patients by Weeks 48 and 96, respectively. However, use of a more sensitive PCR assay detected many of the emerging changes at baseline, suggesting that they originated during LVD therapy. Only a subset of the changes in ETVr isolates altered their susceptibilities, and virtually all isolates were significantly replication impaired in vitro. Consequently, only 2/187 (1%) patients experienced ETVr rebounds in year 1, with an additional 14/151 (9%) patients experiencing ETVr rebounds in year 2. Isolates from all 16 patients with rebounds were LVDr and harbored the T184 and/or S202 change. Seventeen other novel substitutions emerged during ETV therapy, but none reduced the susceptibility to ETV or resulted in a rebound. In summary, ETV was effective in LVD-refractory patients, with resistant sequences arising from a subset of patients harboring preexisting LVDr/ETVr variants and with approximately half of the patients experiencing a virologic rebound.
恩替卡韦(ETV)是一种脱氧鸟苷类似物,已被批准用于治疗野生型和拉米夫定耐药(LVDr)乙型肝炎病毒(HBV)的慢性感染。在拉米夫定难治性患者中,1.0mg恩替卡韦在第48周和第96周时分别使21%和34%的患者的HBV DNA水平降至PCR检测水平以下(<300拷贝/ml)。先前的研究表明,恩替卡韦耐药(ETVr)导致的病毒学反弹需要预先存在的LVDr HBV逆转录酶替代M204V和L180M,以及T184、S202或M250处的额外变化。为了监测耐药情况,对192例接受恩替卡韦治疗患者的可用分离株进行测序,除了对所有经历病毒学反弹患者的分离株进行表型分析外,还对所有出现替代的分离株进行表型分析。在6%的患者中,基线时在LVDr HBV中发现了T184、S202或M250替代,在接受恩替卡韦治疗的患者中,分别在第48周和第96周时,另外11/187(6%)和12/151(8%)的患者的分离株中出现了该替代。然而,使用更敏感的PCR检测方法在基线时检测到了许多新出现的变化,这表明它们起源于拉米夫定治疗期间。只有一部分ETVr分离株的变化改变了它们的敏感性,并且几乎所有分离株在体外的复制都受到显著损害。因此,在第1年只有2/187(1%)的患者出现ETVr反弹,在第2年又有14/151(9%)的患者出现ETVr反弹。所有16例出现反弹患者的分离株均为LVDr,并带有T184和/或S202变化。在恩替卡韦治疗期间还出现了17种其他新的替代,但没有一种降低了对恩替卡韦的敏感性或导致反弹。总之,恩替卡韦在拉米夫定难治性患者中有效,耐药序列源于一部分携带预先存在的LVDr/ETVr变异的患者,约一半的患者出现病毒学反弹。