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1 ith a high barrier to resistance (tenofovir, entecavir).
2 mtricitabine, tenofovir, and, more recently, entecavir.
3 ents showed that M184V confers resistance to entecavir.
4 efovir 15% (5 of 33), tenofovir 0% (0 of 3), entecavir 0% (0 of 1), and 5% (1 of 20) for those not gi
5 eAg-positive CHB patients were randomized to entecavir 0.5 mg (n = 354) or lamivudine 100 mg (n = 355
9 ng-term viral suppression can be obtained by entecavir and tenofovir even in cases of multidrug resis
11 of nucleos(t)ide analogs and agents such as entecavir and tenofovir with high potency and high genet
12 nts including tenofovir disoproxil fumarate, entecavir, and telbivudine offer greater potency than la
16 1-resistance patterns and their selection by entecavir, caution is needed with the use of entecavir i
21 3 years of therapy with telbivudine (LdT) or entecavir (ETV) and to assess predictive factors for eGF
22 omly assigned to receive either prophylactic entecavir (ETV) before chemotherapy to 3 months after co
26 side analog inhibitor of viral DNA synthesis entecavir (ETV) reduced hepatocyte turnover during clear
29 ic antiviral resistance was performed on 673 entecavir (ETV)-treated nucleoside naive hepatitis B vir
32 nfections numerically, whereas tenofovir and entecavir had no cases and may be more effective, but th
33 comparatively high and both telbivudine and entecavir have decreased efficacy against lamivudine-res
34 ore potent nucleoside analogs (tenofovir and entecavir) have proven to have much lower rates of antiv
36 entecavir, caution is needed with the use of entecavir in persons with HIV-1 and HBV coinfection who
40 e obtained supportive in vitro evidence that entecavir is a potent partial inhibitor of HIV-1 replica
44 alysis showed that in one of these patients, entecavir monotherapy led to an accumulation of HIV-1 va
45 s B liver transplant recipients treated with entecavir monotherapy without hepatitis B immune globuli
48 titis B immunoglobulin (HBIG), or lamivudine+entecavir on direct sequencing were cloned after nested
49 resistance as a first-line therapy, such as entecavir or tenofovir, provides the best chance of achi
50 alogues with lower resistance rates, such as entecavir or tenofovir, suppress hepatitis B virus (HBV)
55 ents undergoing HBV-related LT and receiving entecavir plus low-dose, on-demand HBIg were enrolled an
59 esistance mutation V173L (in 5 samples), the entecavir-resistance mutations T184S (in 2 samples) and
61 ucleotide analogs, lamivudine, adefovir, and entecavir, suppress HBV replication and are extremely we
62 assessed the HCC incidence beyond year 5 of entecavir/tenofovir (ETV/TDF) therapy and tried to deter
64 cing of the viral genome was performed on 11 entecavir-treated and pegylated interferon (peginterfero
66 ntigen truncation mutations were detected in entecavir-treated patients with HCC but not in peginterf
69 rmed HBeAg seroconversion occurred in 31% of entecavir-treated versus 25% of lamivudine-treated patie
70 Among patients treated in year 2, 74% of entecavir-treated versus 37% of lamivudine-treated patie
71 polymerase chain reaction (PCR), and 79% of entecavir-treated versus 68% of lamivudine-treated patie
77 dy in chimeric mice harboring the lamivudine/entecavir triple mutant, FMCAP effectively reduced HBV v
78 0M/rtM204V) mutants as well as in lamivudine/entecavir triple mutants (L180M+S202G+M204V) in vitro.
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