ライフサイエンスコーパス: 3TC

1 3TC and FTC are taken up by cells and converted into 3TC

2 3TC has been shown to be more potent and less toxic than

3 (-)3TC is the only analog containing an unnatural l(-) nucl

4 3TC/FTC-resistant mutants (M184V/I) emerged infrequently

5 gic failure was associated with continuing a 3TC-containing regimen.

6 ion of HIV dynamics under the influence of a 3TC D4T Reverse Transcriptase Inhibitors (RTI) drug regi

7 ompared with those who continued receiving a 3TC-containing regimen.

8 -d4C), however, showed cross-resistance to a 3TC-resistant variant (HIV-1(M184V)).

9 ctor of 3, while replication of HIV-1 with a 3TC-resistant RT (M184V) had no significant effect on th

10 or (NRTI) backbone with lamivudine/abacavir (3TC/ABC) as a commonly used alternative.

11 ith zidovudine/lamivudine (3TC) and abacavir/3TC (except triglycerides, which were unchanged).

12 t triglycerides were unchanged with abacavir/3TC).

13 dependent changes in susceptibility to ABC, 3TC, TDF, and didanosine on titration of K65R and/or M18

14 The DTG-ABC-3TC group had a shorter median time to viral suppression

15 No participants in the DTG-ABC-3TC group had detectable antiviral resistance; one tenof

16 g to adverse events was lower in the DTG-ABC-3TC group than in the EFV-TDF-FTC group (2% vs. 10%); ra

17 iter was significantly higher in the DTG-ABC-3TC group than in the EFV-TDF-FTC group (88% vs. 81%, P=

18 plus abacavir-lamivudine once daily (DTG-ABC-3TC group) or combination therapy with efavirenz-tenofov

19 was reported more frequently in the DTG-ABC-3TC group.

20 s from baseline in spine and hip BMD for ABC-3TC versus TDF-FTC were -1.3% and -3.3% (P = .004) and -

21 xty-nine persons randomized to 4 arms of ABC-3TC or TDF-FTC with EFV or ATV/r.

22 s were randomized and blinded to receive ABC-3TC or TDF-FTC with open-label EFV or ATV/r.

23 Compared with ABC-3TC, TDF-FTC-treated participants had significantly grea

24 ABC/3TC and TDF/FTC significantly and similarly decreased fa

25 standard of care: 3-drug regimen of DTG/ABC/3TC.

26 stratum, times to virologic failure for ABC/3TC or TDF/FTC were not different with EFV or ATV/r.

27 ailure rate was significantly higher for ABC/3TC than for TDF/FTC when given with either EFV or ATV/r

28 ime to virologic failure was similar for ABC/3TC vs TDF/FTC with ATV/r (hazard ratio [HR] 1.25, 95% c

29 horter times to regimen modification for ABC/3TC with EFV or ATV/r and to safety events with EFV.

30 r EFV combined with abacavir/lamivudine (ABC/3TC) or tenofovir/emtricitabine (TDF/FTC) in 1857 human

31 02 compared blinded abacavir/lamivudine (ABC/3TC) to tenofovir DF/emtricitabine (TDF/FTC) with efavir

32 nfected subjects to abacavir-lamivudine (ABC/3TC) versus tenofovir DF-emtricitabine (TDF/FTC) with ef

33 tabine (TDF/FTC) or abacavir/lamivudine (ABC/3TC).

34 over time when paired with a backbone of ABC/3TC: 16% per 5 years (95% confidence interval [CI], 4%,

35 Only ABC/3TC-containing regimens were associated with an increase

36 a backbone containing either TDF/FTC or ABC/3TC.

37 Fat mtDNA content decreased within the ABC/3TC and TDF/FTC groups (combining EFV and ATV/r arms; me

38 Differences between the ABC/3TC and TDF/FTC groups were significant for complex I (P

39 10(3)/microg, respectively) but not the ABC/3TC group.

40 Due to higher virologic failure with ABC/3TC in the high HIV RNA stratum, blinded treatment was s

41 r virologic failure rates were seen with ABC/3TC with EFV (HR 2.46, 95% CI 1.20, 5.05) or ATV/r (HR 2

42 With ABC/3TC, women had a significantly higher (32%) safety risk

43 ction regimen of 3 drugs (DTG/abacavir [ABC]/3TC), followed by DTG + 3TC maintenance if virologically

44 ro against HBV, which is also active against 3TC-resistant HBV variants.

45 Discrimination against 3TC-TP is based on the slower rate of incorporation due

46 ensitivity of HIV-1 to the nucleoside analog 3TC was not affected by the level of RT per particle.

47 In contrast, a nucleoside analog (3TC-TP, triphosphate form of lamivudine) is incorporated

48 In the case of the nucleoside analogs 3TC and FTC, resistant viruses are selected with mutatio

49 are rapidly fixed in the presence of A3G and 3TC suggests that A3G-mediated editing can be an importa

50 ibited higher anti-HIV activity than AZT and 3TC against cell-free virus.

51 tant resistant to the combination of AZT and 3TC due to a single, unique point mutation.

52 to the nucleoside analog inhibitors AZT and 3TC.

53 Rather, dCTP and 3TC-TP bind with nearly equal affinities, but the bindin

54 ) were determined for incorporating dCTP and 3TC-TP by wild-type and 3TC-resistant HIV-1 RT.

55 tant were increased for PMEA diphosphate and 3TC triphosphate by 2-3-fold.

56 lutamate derivative containing AZT, FLT, and 3TC (34, EC(50) = 0.9-1.4 muM) exhibited higher anti-HIV

57 Incorporation of FTC and 3TC monophosphate varied up to 10-fold opposite 7 differ

58 me greater later in the dosing interval, and 3TC SP concentrations were substantially greater than BP

59 logic failure accumulated additional Nvp and 3TC mutations plus Rtv and Nfv mutations.

60 Nvp and 3TC mutations were detected frequently at virologic fail

61 hat the K70E mutation confers minor PMEA and 3TC resistance to HIV-1.

62 e supporting the use of coformulated TDF and 3TC/FTC as preferred backbone drugs for PEP.

63 (DXG-TP), 3'-azido-3'-deoxythymidine-TP, and 3TC-TP by using steady state kinetic analysis and the in

64 corporating dCTP and 3TC-TP by wild-type and 3TC-resistant HIV-1 RT.

65 Both the wild-type and 3TC-resistant mutant RT showed higher fidelity using an

66 ell as DNA replication of both wild-type and 3TC-resistant virus.

67 Infants received ZDV and 3TC for 6 weeks and a single dose of oral d4T at weeks 1

68 deoxy-CTP), (+)3TC-triphosphate (TP), and (-)3TC-TP on the polymerase and exonuclease activities of r

69 ase (RT) inhibitor lamivudine (also known as 3TC) is associated with a substitution of valine for met

70 y resistant RT and several drugs (i.e., AZT, 3TC, hydroxyurea, and thymidine) and led to increases in

71 sical mixture containing FLT-succinate, AZT, 3TC, and glutamic acid exhibited 115-fold less activity

72 buting to the strong antiviral effect of AZT-3TC combination therapy.

73 ART regimens were TDF/3TC/EFV (39%) and AZT/3TC/NVP (34%); 49% of pregnancies had prenatal TDF expos

74 ffect was observed with AZT-resistant or AZT/3TC dually resistant RT and several drugs (i.e., AZT, 3T

75 nificantly more virological failure than AZT/3TC/NVP; a third study was terminated prematurely becaus

76 Pol gamma were similar (0.01 s(-)1) for both 3TC analogs.

77 V) was used to select for resistance to both 3TC and PMPA by serial passage in the presence of increa

78 Moreover, chain termination by 3TC and FTC was strongly influenced by template sequence

79 inhibition of HIV-1 reverse transcriptase by 3TC.

80 ry rat hepatocytes and normal rats comparing 3TC and the corresponding HepDirect prodrug demonstrated

81 No effect of prior or concomitant 3TC/FTC was shown.

82 ng that Lys154 may play a role in conferring 3TC sensitivity to HIV-1 RT.

83 ratory toxicities than were those containing 3TC (adjusted HR, 0.78; P = .04).

84 c/mL >/=3 months were randomized to continue 3TC/ABC or switch to FTC/TDF.

85 TC/TDF was noninferior compared to continued 3TC/ABC (86.4% vs 83.3%, treatment difference 3.0% (95%

86 by comparing the effects of dideoxy-CTP), (+)3TC-triphosphate (TP), and (-)3TC-TP on the polymerase a

87 In cell culture (-)3TC is less toxic than its d(+) isomer, (+)3TC, containi

88 (3TC), ZDV/didanosine (ddI), stavudine (d4T)/3TC, d4T/ddI, and ddI/3TC.

89 proved for antiviral therapy: AZT, ddC, D4T, 3TC and carbovir.

90 D4T/3TC, d4T/ddI, and ddI/3TC have similar toxicity rates an

91 lure of stavudine-lamivudine-nevirapine (d4T/3TC/NVP; P < .01), and K103N, V106M, and M184V with fail

92 K103N, V106M, and M184V with failure of d4T/3TC/efavirenz (EFV; P < .01).

93 wer rate of clinical toxicities than was d4T/3TC.

94 istered with AZT (Zidovudine 100 mg/kg/day), 3TC (Lamivudine 50 mg/kg/day) or D4T (Stavudine 10 mg/kg

95 tructure of Pollambda-DNA-D-dCTP, L-dCTP, (-)3TC-TP, and (-)FTC-TP all have their ribose rotated by 1

96 or Zdv, zalcitabine (ddC), didanosine (ddI), 3TC, and stavudine (d4T) were determined, using an enzym

97 se transcriptase enzyme inhibitors AZT, ddI, 3TC, d4T, foscarnet, and nevirapine, as well as the prot

98 linical toxicities than were d4T/ddI and ddI/3TC and with a higher rate of laboratory toxicities than

99 D4T/3TC, d4T/ddI, and ddI/3TC have similar toxicity rates and are appropriate for

100 (ddI), stavudine (d4T)/3TC, d4T/ddI, and ddI/3TC.

101 zidodeoxythymidine (AZT), deoxythiacytidine (3TC), and thymidine was studied using both an intravenou

102 (DTG/abacavir [ABC]/3TC), followed by DTG + 3TC maintenance if virologically suppressed; and (4) sta

103 ost-effectiveness and budget impact of DTG + 3TC regimens in the United States.

104 rison); (2) 2-drug: initial regimen of DTG + 3TC; (3) induction-maintenance: 48-week induction regime

105 Should DTG + 3TC demonstrate high rates of virologic suppression, thi

106 y suppressed patients were switched to DTG + 3TC maintenance.

107 g was the preferred strategy only when DTG + 3TC 48-week virologic suppression rate exceeded 90%.

108 d emergence of M184V mutants of HIV-1 during 3TC therapy of human patients.

109 o acid 515 (L515M) have been observed during 3TC and Famciclovir therapy as well.

110 EFV+FTC-TDF versus 313 (60%) assigned to EFV+3TC-ZDV (HR 0.64, CI 0.54-0.76; p<0.001) and there was a

111 (15%) among 519 participants assigned to EFV+3TC-ZDV (HR 1.51, CI 1.12-2.04; p = 0.007).

112 were hypothesized to be non-inferior to EFV+3TC-ZDV if the upper one-sided 95% confidence bound for

113 DF had similar high efficacy compared to EFV+3TC-ZDV in this trial population, recruited in diverse m

114 Comparing EFV+FTC-TDF to EFV+3TC-ZDV, during a median 184 wk of follow-up there were

115 Comparing ATV+DDI+FTC to EFV+3TC-ZDV, during a median follow-up of 81 wk there were 1

116 th efavirenz plus lamivudine-zidovudine (EFV+3TC-ZDV), atazanavir plus didanosine-EC plus emtricitabi

117 dine [3TC]/zidovudine [ZDV]/efavirenz [EFV], 3TC/ZDV/nelfinavir [NFV], or other regimens) and studied

118 cumulation and/or inhibition of elimination (3TC) are responsible for SP concentrations of these agen

119 This model can also explain 3TC resistance in feline immunodeficiency virus and huma

120 erse transcriptase (RT) evokes the 1000-fold 3TC (Lamivudine) resistance by the HIV-1 virus observed

121 TP substrate but increasing its affinity for 3TC-triphosphate.

122 ted proviruses via recombination allowed for 3TC escape under culture conditions prohibitive for any

123 00 and <100,000 copies/mL who were naive for 3TC and abacavir.

124 in incorporation efficiency was observed for 3TC-MP incorporation by M184V RT for DNA- and RNA-depend

125 (pol) was slower and the K(d) was weaker for 3TC-TP incorporation by the M184V RT, the decrease in th

126 Switching to FTC/TDF from 3TC/ABC maintained virologic suppression, had fewer VFs,

127 Myristoyl-Glu(3TC)-FLT (46, EC(50) = 0.3-0.6 muM) and myristoyl-Glu(FT

128 .06 to 0.0004 s(-1) for the series FIAU > (+)3TC approximately equal to (-)3TC > CBV > AZT > PMPA app

129 didehydro-2',3'-dideoxythymidine (d4T) >> (+)3TC >> (-)3TC > PMPA > azidothymidine (AZT) >> Carbovir

130 2',3'-dideoxythymidine (d4T) >> (+)3TC >> (-)3TC > PMPA > azidothymidine (AZT) >> Carbovir (CBV).

131 and the side chains of Val184 of M184V RT in 3TC-resistant mutant HIV strains destabilizes the RT-nuc

132 lysis reveals that Pol gamma incorporates (-)3TC-triphosphate 16-fold less efficiently than the corre

133 ent with the reverse transcriptase inhibitor 3TC resulted in decreased TE transposition as well as in

134 -)3TC is less toxic than its d(+) isomer, (+)3TC, containing the natural nucleoside configuration, an

135 Virologic outcome among 104 lamivudine (3TC)-experienced individuals infected with human immunod

136 g-term effects of abacavir (ABC)-lamivudine (3TC), compared with tenofovir (TDF)-emtricitabine (FTC)

137 bility to the nucleoside analogs lamivudine (3TC) and tenofovir at both the virus and enzyme levels.

138 , 100, and 200 mg once daily and lamivudine (3TC) 150 mg 2 times/day in 82 human immunodeficiency vir

139 Women received d4T and lamivudine (3TC) from enrollment until labor.

140 ine (d4T), didanosine (ddI), and lamivudine (3TC), and the nucleotide RTI inhibitor tenofovir (TDF),

141 rapy with dolutegravir (DTG) and lamivudine (3TC).

142 fovir (TDF), abacavir (ABC), and lamivudine (3TC); (2) lower fold resistance associated with mixtures

143 zed to ddA) > stavudine (d4T) >> lamivudine (3TC) > tenofovir (PMPA) > zidovudine (AZT) > abacavir (m

144 T) inhibitors (NRTIs), including lamivudine (3TC) and zidovudine (Zdv), are being evaluated for the t

145 reverse transcriptase inhibitors lamivudine (3TC) [(-)-beta-L-2',3'-dideoxy-3'-thiacytidine), FTC (5-

146 th -2'-deoxy-3'-thiacytidine, or lamivudine (3TC), and following orthotopic liver transplantation for

147 ial compared abacavir (ABC) plus lamivudine (3TC) and ZDV+3TC as part of a dual or triple first-line

148 dren given zidovudine (ZDV) plus lamivudine (3TC) as a 2-drug PEP regimen.

149 erent combinations of stavudine, lamivudine (3TC), nevirapine (Nvp), nelfinavir (Nfv), and ritonavir

150 ore TDF-containing regimens: TDF/lamivudine (3TC)/nevirapine (NVP) (n = 3), TDF/ emtricitabine (FTC)/

151 5'-monophosphates of vidarabine, lamivudine (3TC), and cytarabine as well as the phosphonic acid adef

152 he appearance of proviruses with lamivudine (3TC) drug resistance-associated mutations before any dru

153 rus (SIVmac251) and treated with lamivudine (3TC) or emtricitabine [(-)-FTC] (two animals per drug).

154 Treatment of patients with lamivudine (3TC) results in loss of detectable levels of hepatitis B

155 penetration of zidovudine (ZDV), lamivudine (3TC), and amprenavir (APV), given alone and in combinati

156 RT), including zidovudine (ZDV), lamivudine (3TC), and indinavir (IDV), and found a significant incre

157 l treated with zidovudine (ZDV), lamivudine (3TC), and lopinavir-ritonavir (LPV/r), were followed up

158 indinavir (IDV)/zidovudine (ZDV)/lamivudine (3TC), IDV, or ZDV/3TC.

159 mon NRTI pairs: zidovudine (ZDV)/lamivudine (3TC), ZDV/didanosine (ddI), stavudine (d4T)/3TC, d4T/ddI

160 levels increased with zidovudine/lamivudine (3TC) and abacavir/3TC (except triglycerides, which were

161 eive sdNVP and either zidovudine/lamivudine (3TC), tenofovir/emtricitabine (FTC), or lopinavir/ritona

162 hate forms of antiviral drugs lamivudine ((-)3TC-TP) and emtricitabine ((-)FTC-TP) provide little str

163 n-terminating antiviral drugs lamivudine ((-)3TC-TP) and emtricitabine ((-)FTC-TP), we structurally r

164 CTP), or the triphosphates of lamivudine ((-)3TC-TP) and emtricitabine ((-)FTC-TP) with four ternary

165 is B (interferon [IFN]-alpha and lamivudine [3TC]) have limited long-term utility because of side eff

166 antiretroviral therapy regimens (lamivudine [3TC]/zidovudine [ZDV]/efavirenz [EFV], 3TC/ZDV/nelfinavi

167 90.2%-97.7%) and lowest for ZDV+ lamivudine [3TC]+LPV/r (59.1%; 95% CI, 36.2%-82.0%).

168 L-2',3'-dideoxy-3'-thiacytidine (lamivudine, 3TC)] for the treatment of Herpes B virus (HBV) infectio

169 )-2',3'-dideoxy-3'-thiacytidine (lamivudine, 3TC, 1) were synthesized and evaluated for their anti-HI

170 Structural and biochemical analysis of 3TC-resistant HIV-1 reverse transcriptase (RT) led to a

171 esistant to 3TC, AZT, and the combination of 3TC and AZT, confirming the role of the Pro-156-Ser muta

172 oxythymidine (AZT) and to the combination of 3TC and AZT.

173 mergence of resistance to the combination of 3TC plus PMPA.

174 nce of increasing stepwise concentrations of 3TC.

175 nosubstituted 5'-O-fatty acyl derivatives of 3TC (EC(50) = 0.2-2.3 muM) were more potent than the cor

176 account for the strong antiviral efficacy of 3TC versus that of ddC.

177 ng configurations, as with the enantiomer of 3TC that is used in therapy.

178 so resistant to the 5'-triphosphate forms of 3TC, (-)-FTC, and ddC.

179 ere designed to compare the incorporation of 3TC-TP and (-)-FTC-TP into DNA by HIV-1 RT and illuminat

180 understanding of the molecular mechanism of 3TC-drug resistance and supports suggestions that increa

181 cal use of Zdv, ddC, ddI, and d4T but not of 3TC for the antiretroviral treatment of HTLV-1-associate

182 Furthermore, in the presence of 3TC, a known inhibitor of HBV reverse transcriptase, yea

183 nts was resistant to the 5'-triphosphates of 3TC and AZT.

184 -7-fold resistant to the 5'-triphosphates of 3TC, FTC, and AZT.

185 onversely, the more effective excision of (-)3TC, CBV, and AZT may contribute to lower toxicity.

186 conformation, following incorporation of (-)3TC-MP, with a second (-)3TC-TP molecule bound to the ac

187 h HIV-1 CRF02_AG, 8 treatment-naive and 4 on 3TC-AZT-NVP] showed 3 to 4 mutations in the Gag P2/NC CS

188 of FTC than with the lower FTC doses and/or 3TC (P=.02, P=.04, and P=.04, respectively).

189 Low-frequency NVP- or 3TC/FTC-resistant mutants at codons 103, 181, and 184 we

190 )-2', 3'-dideoxy-3'-thiacytidine [(-)SddC or 3TC] is the only analogue with the unnatural L(-) nucleo

191 During labor, women received oral 3TC and either intravenous or oral d4T.

192 essed on a boosted protease inhibitor (PI) + 3TC/ABC regimen, the merits of switching to FTC/TDF as t

193 Individuals who received 3TC/ZDV/EFV had a more rapid phase 1 viral decay rate th

194 e 1 viral decay rate than those who received 3TC/ZDV/NFV or other regimens.

195 Subjects receiving 3TC/ABC + PI + ritonavir (RTV) with HIV-1 RNA < 200 c/mL

196 155 to PI + RTV + FTC/TDF, 156 to PI + RTV + 3TC/ABC).

197 incorporation of (-)3TC-MP, with a second (-)3TC-TP molecule bound to the active site in the absence

198 At baseline, all patients were taking 3TC or FTC and were hepatitis B surface antigen and hepa

199 TDF/3TC/EFV was equivalent to its comparator arms.

200 TDF/3TC/NVP was the least well-studied and appeared the leas

201 ), TDF/ emtricitabine (FTC)/NVP (n = 9), TDF/3TC/efavirenz (EFV) (n = 6), and TDF/FTC/EFV (n = 19).

202 Further study of TDF/3TC/NVP is required before it is widely deployed for ini

203 In 2 comparative studies, TDF/3TC/NVP was associated with significantly more virologic

204 The most frequent ART regimens were TDF/3TC/EFV (39%) and AZT/3TC/NVP (34%); 49% of pregnancies

205 In contrast, removal of 3'-terminal 3TC residues was 50% as efficient as natural 3' termini.

206 s incorporated 10-fold more efficiently than 3TC-TP during HIV-1 RT-catalyzed RNA-dependent DNA synth

207 at (-)-FTC is 6- to 10-fold more potent than 3TC.

208 3TC/ZDV/EFV regimen may be more potent than 3TC/ZDV/NFV or other regimens and that early viral dynam

209 P by two orders of magnitude better than (-)-3TC-TP.

210 These findings show that 3TC and Famciclovir selected mutations alter the propert

211 Recent studies have shown that 3TC resistance mutations, including M184I, increase the

212 The 3TC-resistant HIV-1 RT showed a similar efficiency of in

213 The model can also explain the 3TC resistance of analogous hepatitis B polymerase mutan

214 bstantially reduced binding affinity for the 3TC-TP to the enzyme.DNA (or RNA) complex poised for DNA

215 We have determined crystal structures of the 3TC-resistant mutant HIV-1 RT (M184I) in both the presen

216 ped a model that explains the ability of the 3TC-resistant mutant M184I to incorporate dNTPs but not

217 Our findings indicate that the 3TC/ZDV/EFV regimen may be more potent than 3TC/ZDV/NFV

218 in, (-)beta-L-2',3'-dideoxy-3'-thiacytidine (3TC [lamivudine]), and famciclovir (oral prodrug of penc

219 and (-)beta-L-2',3'-dideoxy-3'-thiacytidine (3TC) (M184V) remain sensitive to DXG.

220 nd (-)-beta-L-2',3'-dideoxy-3'-thiacytidine (3TC) and additionally exhibited low-level resistance to

221 eoside analog 2',3'-dideoxy-3'-thiacytidine (3TC) is a potent inhibitor of wild-type human immunodefi

222 ide analog (-)-2', 3'-deoxy-3'-thiacytidine (3TC) leads to the development of resistance-conferring m

223 isition of (-)2',3'-dideoxy-3'-thiacytidine (3TC) resistance in vitro.

224 ifically for 2', 3'-dideoxy-3'-thiacytidine (3TC) triphosphate.

225 addition, (-)2',3'-dideoxy-3'-thiacytidine (3TC) was also found to increase the mutation rate of HIV

226 ug beta-l-(-)-2',3'-dideoxy-3'-thiacytidine (3TC) was difficult to remove by pyrophosphorolysis, in c

227 t to (-)-beta-2',3'-dideoxy-3'-thiacytidine (3TC) were selected by culturing virus in the presence of

228 s of (-)-beta-2',3'-dideoxy-3'-thiacytidine (3TC), (-)-beta-2',3'-dideoxy-5-fluoro-3'-thiacytidine (F

229 ), (-)-beta-L-2',3'-dideoxy-3'-thiacytidine (3TC), (-)-beta-L-2',3'-dideoxy-5-fluorocytidine (FddC),

230 ine (AZT), (-)2',3'-dideoxy-3'-thiacytidine (3TC), and AZT-resistant HIV-1 reverse transcriptase (RT)

231 nalog inhibitor, 3'-dideoxy 3'-thiacytidine (3TC), implying that Lys154 may play a role in conferring

232 evirapine and 2',3'-dideoxy-3'-thiacytidine (3TC), respectively.

233 ides (-)-beta-2',3'-dideoxy-3'-thiacytidine (3TC)--an approved anti-human immunodeficiency virus (HIV

234 t to create a 2',3'-dideoxy-3'-thiacytidine (3TC)-sensitive virus, the second residue in the highly c

235 eoside analog 2',3'-dideoxy-3'-thiacytidine (3TC).

236 IDS, (-)-beta-2',3'-dideoxy-3'-thiacytidine (3TC, lamivudine) is the only one with the unnatural (-)-

237 S therapy is 2', 3'-dideoxy-3'-thiacytidine (3TC, lamivudine).

238 (D4T-TP), (-)-2',3'-dideoxy-3'-thiacytidine (3TC-TP), and carbocyclic 2',3'-didehydro-ddGTP (CBV-TP)

239 resistance to (-)-2'-deoxy-3'-thiacytidine (3TC; lamivudine) and increased sensitivity to 9-[2-(phos

240 beta-d-(+)-2',3'-dideoxy-3'-thiacytidine ((-)3TC])).

241 beta-L-(-)-2',3'-dideoxy-3'-thiacytidine (-)3TC, and (R)-9-(2-phosphonylmethoxypropyl)adenine (PMPA)

242 og, lamivudine [(-)2'-deoxy-3'-thiacytidine, 3TC].

243 dine, [(-)-2,3'-dideoxy-3'-thiacytidine, (-)-3TC] are both potent RT inhibitors, but Pol gamma discri

244 complex (M184I/DNA/3TCTP) and contribute to 3TC resistance by interfering with the formation of a ca

245 omplex, which causes the cross-resistance to 3TC (M184V mutant).

246 e (RT) in HIV cause high-level resistance to 3TC and contribute to the failure of anti-AIDS combinati

247 ce involves enhanced excision, resistance to 3TC involves a block to incorporation of the analog.

248 Virus resistance to 3TC is associated with mutations which lead to amino aci

249 In contrast, high-level resistance to 3TC was found in all HTLV-1 isolates.

250 type 1 (HIV-1) is selected for resistance to 3TC, the methionine normally present at position 184 is

251 ite-directed mutants displayed resistance to 3TC, thus confirming the role of these mutations in the

252 F-4'Sd4FC 35 showed high cross-resistance to 3TC-resistant mutant (M184V) RT.

253 sily detected the evolution of resistance to 3TC.

254 MLV RT confer a high level of resistance to 3TC.

255 site, leads to a high level of resistance to 3TC.

256 n this Pro-156-Ser mutation was resistant to 3TC, AZT, and the combination of 3TC and AZT, confirming

257 3M mutant RT is also relatively resistant to 3TC.

258 ition of the YXDD motif are all resistant to 3TC.

259 3 mutants of MLV RT were highly resistant to 3TC.

260 and both of these mutants were resistant to 3TC.

261 ries FIAU > (+)3TC approximately equal to (-)3TC > CBV > AZT > PMPA approximately equal to d4T >> ddA

262 as natural deoxynucleotides, whereas AZT-TP, 3TC-TP, and CBV-TP were only moderate inhibitors of DNA

263 e and the superior antiviral activity versus 3TC of the 200 mg/day FTC dose confirmed the results of

264 ellular half-life of FTC-triphosphate versus 3TC-triphosphate.

265 copies/mL, 86% were HBeAg positive, 94% were 3TC resistant, median serum ALT was 52 IU/L, and 98% had

266 We sought to determine whether 3TC can inhibit the replication of wild-type murine leuk

267 cohort of 6 HIV coinfected subjects for whom 3TC and IFN therapy had previously failed.

268 Treatment for up to 36 days with 3TC reduced the amount of cccDNA in the cultures not mor

269 emonstrate that the combination of PMPA with 3TC or (-)-FTC selects for the K65R mutation and against

270 in effects similar to that of treatment with 3TC.

271 Prior treatment with 3TC/FTC does not compromise efficacy of TDF treatment.

272 The use of combination treatment with 3TC/FTC offers no significant benefit over TDF alone.

273 d4T with or without 3TC is a potential alternative to ZDV for HIV-infected p

274 abacavir (ABC) plus lamivudine (3TC) and ZDV+3TC as part of a dual or triple first-line antiretrovira

275 (1.9%; 95% CI, 0%-3.8%) and highest for ZDV+3TC+boosted atazanavir (21.2%; 95% CI, 13.5%-30.0%).

276 This review supports ZDV+3TC+LPV/r as the preferred 3-drug regimen for PEP in chi

277 We conclude that the combination of ZDV, 3TC, and LPV/r is able to provide efficient and durable

278 y preterm birth, and neonatal death; and ZDV-3TC-LPV-R was associated with higher risk for preterm bi

279 -1.52); zidovudine, lamivudine, and NPV (ZDV-3TC-NVP) (647 of 1365 [47.4%]; ARR, 1.30; 95% CI, 1.20-1

280 7.4%]; ARR, 1.30; 95% CI, 1.20-1.41); or ZDV-3TC-LPV-R (75 of 167 [44.9%]; ARR, 1.21; 95% CI, 1.01-1.

281 ere associated with higher risk for SGA; ZDV-3TC-NVP was associated with higher risk of stillbirth, v

282 ZDV/3TC was associated with a lower rate of clinical toxicit

283 dovudine (ZDV)/lamivudine (3TC), IDV, or ZDV/3TC.

284 tion of therapy or in those treated with ZDV/3TC alone, who had viral loads in their lymph nodes indi

285 At week 96, patients receiving zidovudine/3TC had lost limb fat, and those receiving emtricitabine