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1 e of ARC-520 and daily nucleosidic analogue (entecavir).
2 ith a high barrier to resistance (tenofovir, entecavir).
3 ting anti-HBV compounds such as tenofovir or entecavir.
4 wed by 40 weeks of combined peginteferon and entecavir.
5 ing pocket for a known anti-HBV drug, namely entecavir.
6 75 patients, 82% Asian, and 55% treated with entecavir.
7 mtricitabine, tenofovir, and, more recently, entecavir.
8 ents showed that M184V confers resistance to entecavir.
9 efovir 15% (5 of 33), tenofovir 0% (0 of 3), entecavir 0% (0 of 1), and 5% (1 of 20) for those not gi
10 eAg-positive CHB patients were randomized to entecavir 0.5 mg (n = 354) or lamivudine 100 mg (n = 355
11 N) (male: <= 45, female: <= 30 U/L) received entecavir 0.5 mg daily for 8 weeks followed by the addit
17 mine the safety and efficacy of therapy with entecavir and peginterferon in a group of children in th
18 he safety and efficacy of the combination of entecavir and peginterferon in adults in the IT phase of
20 ng-term viral suppression can be obtained by entecavir and tenofovir even in cases of multidrug resis
22 of nucleos(t)ide analogs and agents such as entecavir and tenofovir with high potency and high genet
23 a high genetic barrier to resistance, namely entecavir and tenofovir, has improved the efficacy of an
25 nts including tenofovir disoproxil fumarate, entecavir, and telbivudine offer greater potency than la
29 ding the clinical efficacy of switching from entecavir-brand-name drugs (ETV-Brand) to entecavir gene
31 1-resistance patterns and their selection by entecavir, caution is needed with the use of entecavir i
35 with reduced viremia after administration of entecavir, developed polyfunctional, HBV-specific CD8(+)
37 verse transcriptase (RT) inhibitors, such as entecavir (ETV) and lamivudine (3TC), serve as crucial a
39 3 years of therapy with telbivudine (LdT) or entecavir (ETV) and to assess predictive factors for eGF
40 omly assigned to receive either prophylactic entecavir (ETV) before chemotherapy to 3 months after co
46 side analog inhibitor of viral DNA synthesis entecavir (ETV) reduced hepatocyte turnover during clear
50 ic antiviral resistance was performed on 673 entecavir (ETV)-treated nucleoside naive hepatitis B vir
53 had previously been treated with 8 weeks of entecavir followed by 40 weeks of combined peginteferon
54 Conclusion: A lead-in strategy of 8 weeks of entecavir followed by combination peginterferon and ente
56 om entecavir-brand-name drugs (ETV-Brand) to entecavir generic drugs (ETV-Generic) with 0.5 mg once d
58 nfections numerically, whereas tenofovir and entecavir had no cases and may be more effective, but th
60 comparatively high and both telbivudine and entecavir have decreased efficacy against lamivudine-res
61 ore potent nucleoside analogs (tenofovir and entecavir) have proven to have much lower rates of antiv
62 nal safety between tenofovir alafenamide and entecavir; however, the relatively small sample size and
64 entecavir, caution is needed with the use of entecavir in persons with HIV-1 and HBV coinfection who
70 e obtained supportive in vitro evidence that entecavir is a potent partial inhibitor of HIV-1 replica
72 nucleos(t)ide analogue agents, tenofovir and entecavir, is a crucial intervention that supports the g
74 The observed continuous HBV DNA decline is entecavir mediated, the strong but transient HBsAg and H
77 alysis showed that in one of these patients, entecavir monotherapy led to an accumulation of HIV-1 va
78 s B liver transplant recipients treated with entecavir monotherapy without hepatitis B immune globuli
81 titis B immunoglobulin (HBIG), or lamivudine+entecavir on direct sequencing were cloned after nested
82 atures of chronic hepatitis B (CHB) received entecavir once-daily in a dose of 0.015 mg/kg (0.5 mg ma
85 liver transplant recipients receiving either entecavir or tenofovir alafenamide, to assess the effect
87 sis and with chronic hepatitis B who started entecavir or tenofovir treatment with baseline HBV viral
89 resistance as a first-line therapy, such as entecavir or tenofovir, provides the best chance of achi
90 alogues with lower resistance rates, such as entecavir or tenofovir, suppress hepatitis B virus (HBV)
95 ents undergoing HBV-related LT and receiving entecavir plus low-dose, on-demand HBIg were enrolled an
97 ate insurance examines trends in the cost of entecavir prescribed for chronic hepatitis B treatment.
100 esistance mutation V173L (in 5 samples), the entecavir-resistance mutations T184S (in 2 samples) and
101 ults with combined peginterferon alfa-2a and entecavir results in a decline in serum HBeAg and HBsAg
103 purine analogs, nelarabine, fludarabine, and entecavir, showing the suppression of HIV-1 expression f
105 ucleotide analogs, lamivudine, adefovir, and entecavir, suppress HBV replication and are extremely we
106 assessed the HCC incidence beyond year 5 of entecavir/tenofovir (ETV/TDF) therapy and tried to deter
107 notolerant trial participants on PegIFNalpha/entecavir therapy and 88 immune active trial participant
108 ir followed by combination peginterferon and entecavir therapy for 40 weeks had limited efficacy in a
111 cing of the viral genome was performed on 11 entecavir-treated and pegylated interferon (peginterfero
112 enofovir-treated and 25.7% patients who were entecavir-treated had unquantifiable HBV RNA (P > 0.05).
114 ntigen truncation mutations were detected in entecavir-treated patients with HCC but not in peginterf
117 rmed HBeAg seroconversion occurred in 31% of entecavir-treated versus 25% of lamivudine-treated patie
118 Among patients treated in year 2, 74% of entecavir-treated versus 37% of lamivudine-treated patie
119 polymerase chain reaction (PCR), and 79% of entecavir-treated versus 68% of lamivudine-treated patie
122 We demonstrated that in 2 PXB-mice after entecavir treatment, the total cccDNA content did not ch
126 Structural comparison with the DNA:dGTP/entecavir-triphosphate complex also indicated that the c
127 dy in chimeric mice harboring the lamivudine/entecavir triple mutant, FMCAP effectively reduced HBV v
129 0M/rtM204V) mutants as well as in lamivudine/entecavir triple mutants (L180M+S202G+M204V) in vitro.
132 s prior to his consultation, antiviral agent entecavir was commenced for his chronic hepatitis B infe