ライフサイエンスコーパス: NRTI

1 NRTI resistance-associated mutations were reported in fo

2 NRTI triphosphates (NRTI-TP), the biologically active fo

3 NRTI-sensitive DNA polymerases localizing to mitochondri

4 NRTI-triphosphates (NRTI-TP) compete with endogenous 2'-

5 NRTIs and, specifically tenofovir at therapeutic concent

6 NRTIs based on the carbocyclic pseudosugar may offer an

7 NRTIs were efficacious in mouse models of geographic atr

8 In HIV-1, NRTI resistance-associated mutations either reduce RT-me

9 HBV obtained from 20 plasma samples from 11 NRTI-treated patients and 17 plasma samples from 17 NRTI

10 eated patients and 17 plasma samples from 17 NRTI-naive patients, by using standard direct PCR sequen

11 sistance mutations, compared to the use of 2 NRTIs plus 1 NNRTI.

12 aimed to examine whether first-line use of 2 NRTIs plus a boosted protease inhibitor (bPI) could prot

13 itial regimens consisting of an InSTI plus 2 NRTIs.

14 eks of initial antiretroviral therapy with 2 NRTIs and a protease inhibitor (PI) were enrolled.

15 bitors or boosted protease inhibitors with 2 NRTIs.

16 ce of SDRMs was 11.0%, NNRTI mutations 8.2%, NRTI mutations 4.5%, and PI mutations 0.4%.

17 nucleoside RT inhibitor (NRTI)-naive and 252 NRTI-treated persons; and integrase (IN) sequences from

18 reverse transcriptase inhibitor (NNRTI) or 3 NRTIs as long-term ART.

19 oside reverse-transcriptase inhibitor (43%), NRTI plus integrase strand transfer inhibitor (25%), and

20 ere not detected by PCR in 10 samples from 5 NRTI-treated patients, including the lamivudine-resistan

21 Dual TDR to PI and NRTI was seen in 1.6%, NRTI and NNRTI in 3.4%, and triple class TDR in 0.9%.

22 ipants, NNRTI mutation prevalence was 83.6%, NRTI 67.8%, and PI 1.8%.

23 We demonstrate that the probability a NRTI instead of a natural nucleotide is included can be

24 %) of 112 patients with one predicted-active NRTI had viral suppression (p=0.3) and 20 (77%) of 26 pa

25 Compared with results with no active NRTIs, 95 (85%) of 112 patients with one predicted-activ

26 protease inhibitor with no predicted-active NRTIs had viral suppression (viral load <400 copies per

27 77%) of 26 patients with two or three active NRTIs had viral suppression (p=0.08).

28 g 360 participants randomized to omit or add NRTIs, 70% and 65% had HIV-1 RNA <200 copies/mL, respect

29 d regimen and were randomized to omit or add NRTIs.

30 ipants were randomly assigned to omit or add NRTIs.

31 the omit-NRTIs group versus 25.9% in the add-NRTIs group (difference, 3.2 percentage points [95% CI,

32 RTIs group compared with 7 deaths in the add-NRTIs group.

33 A median of 1.0 (IQR 0.0,1.5) additional NRTI mutation accumulated over 2 years' rebound.

34 l viremia did not change significantly after NRTI discontinuation among those without virologic failu

35 r, the emergence of viral resistance against NRTIs is a major threat to their therapeutic effectivene

36 All NRTIs had low toxicity and good clinical, immunological,

37 starting ART with dolutegravir (DTG) and an NRTI pair.

38 Meanwhile, an NRTI, lamivudine, improves insulin sensitivity and reduc

39 of RT, and the nucleoside/nucleotide analog (NRTI) and non-nucleoside (NNRTI) drugs used in treating

40 Eight nucleoside/nucleotide analogs (NRTIs) and five non-nucleoside inhibitors (NNRTIs) are a

41 tegrase strand transfer inhibitor (25%), and NRTI plus protease inhibitor (19%).

42 es in patients in the protease inhibitor and NRTI group and calculated the predicted activity of pres

43 f 426 patients in the protease inhibitor and NRTI group.

44 High levels of NNRTI and NRTI DRMs among CLHIV receiving ABC/3TC/LPV/r suggests a

45 The degree of NNRTI and NRTI resistance after first-line virologic failure was a

46 Dual TDR to PI and NRTI was seen in 1.6%, NRTI and NNRTI in 3.4%, and tripl

47 DRMs to NNRTIs and NRTIs were found among 65% and 51% of all CLHIV, respect

48 age (P = .009) and the total duration on any NRTI (P = .01).

49 sm of action that is different from approved NRTIs.

50 Importantly, BOX5 attenuated NRTI-induced cytokine up-regulation.

51 ovir plus lamivudine), and D (best available NRTIs plus ritonavir-boosted darunavir plus raltegravir)

52 tion of DNA, thus suppressing excision-based NRTI resistance and also offset the effect of NNRTI resi

53 The relationship between NRTI, reduced telomerase activity, and accelerated aging

54 I (NNRTI) mutations; and 30 (66.7%) had both NRTI and NNRTI mutations.

55 ferences in drug-resistance patterns in both NRTI and NNRTI were observed by site.

56 Prior exposure to both NRTI and NNRTI and confirmed virologic failure on a PI-c

57 onotherapy is generally not recommended, but NRTI-sparing approaches may be considered.

58 /ml were much less likely to resuppress, but NRTI resistance increased only slowly.

59 Estimates differed by NRTI backbone.

60 The inhibition of HK2 infectivity by NRTIs appears to take place at either the reverse transc

61 f K65R, Q151M, and M184V conferred classwide NRTI resistance.

62 ed a search for regimens that do not contain NRTIs.

63 s complete injectable LA regimens containing NRTIs.

64 virine, respectively, independent of current NRTI backbones.

65 These data suggest that current NRTI-based regimens are suboptimal for treating HIV-2 in

66 vel bifunctional RT inhibitor utilizing d4T (NRTI) and a TMC-derivative (a diarylpyrimidine NNRTI) li

67 witched to ATV/RTV at entry and discontinued NRTIs after 6 weeks.

68 dolutegravir in combination with fixed-dose NRTIs represents an effective new treatment option for H

69 y which CN and RH mutations can exhibit dual NRTI and NNRTI resistance.

70 Cabotegravir plus dual NRTI therapy had potent antiviral activity during the in

71 otegravir groups were changed over from dual NRTIs to rilpivirine at week 24, 149 (82%; 95% CI 77-88)

72 iral activity similar to efavirenz plus dual NRTIs until the end of week 96.

73 In pregnant mice, PI-based cART but not dual-NRTI therapy was associated with significantly lower pro

74 ced patients, previously reported to enhance NRTI resistance, also reduce RNase H cleavage and enhanc

75 -dependent pyrophosphorolysis, which excises NRTIs from the end of viral DNA.

76 In settings with extensive NRTI resistance but no available resistance testing, our

77 se H domains of RT in HIV-2 patients failing NRTI-containing therapies.

78 -1 or hepatitis B (adjusted hazard ratio for NRTI exposure, 0.673; 95% confidence interval, 0.638 to

79 nd interactions at position 70, required for NRTI excision.

80 Although TDR was highest for NRTIs, the impact of baseline drug resistance patterns o

81 The first-generation NRTIs, including 2',3'-dideoxycytidine (ddC), were origi

82 resistance (5.8%), baseline genotype guides NRTI selection and informs subsequent ART after adverse

83 Treatment-naive subjects harboring NRTI-DRMs had significantly lower CD4 cells than those w

84 is an appropriate alternative, especially if NRTI use is limited by toxicity.

85 ide has the potential to become an important NRTI backbone.

86 vel K65R of unknown clinical significance in NRTI-naive subtype C-infected women and infants at frequ

87 Open-label optimized regimens (not including NRTIs) were selected on the basis of treatment history a

88 nts) received an optimized regimen including NRTIs.

89 sequences from 333 nucleoside RT inhibitor (NRTI)-naive and 252 NRTI-treated persons; and integrase

90 nucleoside reverse transcriptase inhibitor (NRTI) backbone among their recommended and alternative f

91 nucleoside reverse transcriptase inhibitor (NRTI) backbone with lamivudine/abacavir (3TC/ABC) as a c

92 nucleoside reverse transcriptase inhibitor (NRTI) backbone.

93 nucleoside reverse transcriptase inhibitor (NRTI) backbones (zidovudine, stavudine, tenofovir, or ab

94 nucleoside reverse transcriptase inhibitor (NRTI) cross-resistance mutations (26% vs 13%, P = .23).

95 nucleoside reverse transcriptase inhibitor (NRTI) designed to maintain in-vitro antiviral activity w

96 nucleoside reverse transcriptase inhibitor (NRTI) emtricitabine (FTC), and injectable aqueous nanodi

97 nucleoside reverse transcriptase inhibitor (NRTI) in fixed-dose combination.

98 nucleoside reverse transcriptase inhibitor (NRTI) is tenofovir.

99 nucleoside reverse transcriptase inhibitor (NRTI) mutation in human immunodeficiency virus type 1 (H

100 nucleoside reverse transcriptase inhibitor (NRTI) mutations (4.5%), followed by nonnucleoside revers

101 nucleoside reverse-transcriptase inhibitor (NRTI) mutations; 33 (73%) had non-NRTI (NNRTI) mutations

102 /nucleotide reverse-transcriptase inhibitor (NRTI) plus nonnucleoside reverse-transcriptase inhibitor

103 nucleotide reverse-transcriptase inhibitor (NRTI) resistance in hepatitis B virus (HBV) are not well

104 /nucleotide reverse transcriptase inhibitor (NRTI) resistance, 9.8% had nonnucleoside reverse-transcr

105 nucleoside reverse transcriptase inhibitor (NRTI) SDRMs accounted for >69% of NRTI-associated TDR in

106 nucleoside reverse transcriptase inhibitor (NRTI) selection.

107 nucleoside reverse transcriptase inhibitor (NRTI) therapy.

108 nucleoside reverse transcriptase inhibitor (NRTI), 2',3'-dideoxycytidine or 2',3'-dideoxyinosine, mt

109 nucleoside reverse transcriptase inhibitor (NRTI)-based ART, and HIV-negative controls.

110 nucleoside reverse-transcriptase inhibitor (NRTI)-sparing benefits, low pill burden, once-daily dosa

111 nucleoside reverse-transcriptase inhibitor [NRTI] group) or lopinavir-ritonavir plus zidovudine-lami

112 leos(t)ide reverse transcriptase inhibitors (NRTI) may contribute to accelerated aging in HIV-infecte

113 Nucleoside reverse transcriptase inhibitors (NRTI) require intracellular phosphorylation, which invol

114 Nucleoside reverse-transcriptase inhibitors (NRTI), drugs approved to treat HIV-1 and hepatitis B inf

115 While nucleoside RT inhibitors (NRTIs) are DNA chain terminators, the nucleotide-competi

116 , 4.1% to 8.1% for nucleoside RT inhibitors (NRTIs), and 3.6% to 5.2% for protease inhibitors.

117 Is) and nucleoside/nucleotide RT inhibitors (NRTIs).

118 oside reverse transcriptase (RT) inhibitors (NRTIs) and protease inhibitors designed for HIV-1.

119 oside reverse transcriptase (RT) inhibitors (NRTIs) are the backbone of current antiretroviral treatm

120 nucleoside reverse transcriptase inhibitors (NRTIs and NNRTIs).

121 nucleoside reverse transcriptase inhibitors (NRTIs and NNRTIs).

122 nucleoside reverse transcriptase inhibitors (NRTIs) and a non-nucleoside reverse transcriptase inhibi

123 nucleoside reverse transcriptase inhibitors (NRTIs) and had at least 24 weeks of follow-up after VF.

124 nucleoside reverse transcriptase inhibitors (NRTIs) and non-NRTIs and confirmed virologic failure on

125 nucleoside reverse transcriptase inhibitors (NRTIs) and nonnucleoside reverse transcriptase inhibitor

126 Nucleoside reverse transcriptase inhibitors (NRTIs) are employed in first line therapies for the trea

127 Nucleoside reverse transcriptase inhibitors (NRTIs) are mainstay therapeutics for HIV that block retr

128 Nucleoside reverse transcriptase inhibitors (NRTIs) are often included in antiretroviral regimens in

129 nucleotide reverse transcriptase inhibitors (NRTIs) are recommended as first-line treatment for HIV,

130 ide analog reverse transcriptase inhibitors (NRTIs) are the essential components of highly active ant

131 nucleoside reverse-transcriptase inhibitors (NRTIs) are uncertain when these agents are used with a p

132 Nucleoside reverse transcriptase inhibitors (NRTIs) are widely used as antiviral and anticancer agent

133 nucleoside reverse transcriptase inhibitors (NRTIs) can be safely omitted from salvage therapy as lon

134 nucleoside reverse transcriptase inhibitors (NRTIs) for 24 weeks of induction.

135 nucleoside reverse transcriptase inhibitors (NRTIs) for treatment of HIV infection.

136 nucleoside reverse transcriptase inhibitors (NRTIs) in adults in whom previous first-line antiretrovi

137 nucleoside reverse-transcriptase inhibitors (NRTIs) in first-line antiretroviral therapy (ART) in Afr

138 nucleoside reverse-transcriptase inhibitors (NRTIs) in second-line therapy for patients with HIV, but

139 nucleoside reverse transcriptase inhibitors (NRTIs) involves reverse transcriptase (RT) mutations tha

140 ide analog reverse transcriptase inhibitors (NRTIs) is an important strategy for clinical investigati

141 nucleoside reverse-transcriptase inhibitors (NRTIs) on fat mitochondrial DNA (mtDNA) content and func

142 nucleoside reverse transcriptase inhibitors (NRTIs) or nonnucleoside reverse transcriptase inhibitors

143 nucleoside reverse transcriptase inhibitors (NRTIs) plus an integrase strand transfer inhibitor (InST

144 nucleoside reverse-transcriptase inhibitors (NRTIs) second-line combination after 144 weeks of follow

145 leos(t)ide reverse transcriptase inhibitors (NRTIs) were continued for median nine days after NNRTI i

146 Nucleoside reverse transcriptase inhibitors (NRTIs) were the first drugs used to treat human immunode

147 nucleoside reverse-transcriptase inhibitors (NRTIs) with a nonnucleoside reverse-transcriptase inhibi

148 Nucleoside reverse transcriptase inhibitors (NRTIs) with L-stereochemistry have long been an effectiv

149 nucleotide reverse-transcriptase inhibitors (NRTIs) with or without T-20 and either CPI/r or once-dai

150 nucleoside reverse-transcriptase inhibitors (NRTIs), 4 non-nucleoside reverse transcriptase inhibitor

151 nucleoside reverse transcriptase inhibitors (NRTIs), and protease inhibitors (PIs) using Stanford HIV

152 nucleoside reverse transcriptase inhibitors (NRTIs), and protease inhibitors.

153 nucleoside reverse transcriptase inhibitors (NRTIs), nonnucleoside reverse transcriptase inhibitors (

154 nucleoside reverse transcriptase inhibitors (NRTIs), the most commonly used anti-HIV drugs, compete a

155 nucleotide reverse transcriptase inhibitors (NRTIs).

156 nucleoside reverse-transcriptase inhibitors (NRTIs).

157 nucleoside reverse transcriptase inhibitors (NRTIs).

158 nucleoside reverse-transcriptase inhibitors (NRTIs).

159 nucleoside reverse transcriptase inhibitors (NRTIs; abacavir/lamivudine or tenofovir disoproxil fumar

160 nucleoside reverse transcriptase inhibitors [NRTIs] and nonnucleoside reverse transcriptase inhibitor

161 nucleoside reverse transcriptase inhibitors [NRTIs] plus ritonavir-boosted darunavir plus raltegravir

162 To obtain insight into NRTI resistance, we used a new sequencing technology to

163 PI group) or abacavir/zidovudine/lamivudine (NRTI group) in a clinical trial to prevent mother-to-chi

164 lure has limited the efficacy of second-line NRTI-based regimens in Africa.

165 predicted activity of prescribed second-line NRTIs.

166 ngs for the purpose of selecting second-line NRTIs.

167 ants remaining on the same regimen had lower NRTI resistance rates (11% vs 30%; P = .003) and higher

168 ologic failure detection may result in lower NRTI resistance.

169 PI-based regimens in selection of any major NRTI resistance mutation (crude unweighted prevalence 3.

170 and reproducibility to successfully measure NRTI-TP and dNTP in human PBM cells and macrophages.

171 mpeding the development of excision-mediated NRTI resistance.

172 risk of resistance-related failure of NNRTI/NRTI second-line regimens.

173 t least 24 weeks on a regimen based on a non-NRTI inhibitor were randomly assigned (1:1) to receive o

174 ported in four (2%) of 198 patients, and non-NRTI mutations in 17 (9%) of 198 patients receiving BMS-

175 inhibitor (NRTI) mutations; 33 (73%) had non-NRTI (NNRTI) mutations; and 30 (66.7%) had both NRTI and

176 011) and HIV-infected patients receiving non-NRTI-containing cART (n = 11; P < .001).

177 e those who were no longer responding to non-NRTI-based first-line ART, as assessed with WHO criteria

178 rse transcriptase inhibitors (NRTIs) and non-NRTIs and confirmed virologic failure on a protease inhi

179 Unresolved nonadherence, not NRTI resistance, drives early second-line failure.

180 We analyzed novel NRTIs for their ability to inhibit DNA synthesis of exci

181 structural scaffold for development of novel NRTIs with lower toxicity.

182 ir-ritonavir) plus clinician-selected NRTIs (NRTI group, 426 patients), a protease inhibitor plus ral

183 cts HIV-1 susceptibility to both nucleoside (NRTIs) and non-nucleoside RT inhibitors (NNRTIs) when co

184 nevirapine or efavirenz, whereas only 27% of NRTI SDRMs were associated with high-level resistance to

185 G/N/T accounted for 82.9%, 7.3%, and 1.4% of NRTI-associated TDR, respectively.

186 inhibitor (NRTI) SDRMs accounted for >69% of NRTI-associated TDR in all regions and subtypes.

187 Absence of NRTI mutations and subtherapeutic ART preswitch were ass

188 event NNRTI-RAMs, but increased detection of NRTI-RAMs (OR 4.25; 95% CI 1.02, 17.77; p = 0.03).

189 ratory abnormality before discontinuation of NRTI assignment.

190 tor (bPI) could protect against emergence of NRTI resistance mutations, compared to the use of 2 NRTI

191 uld not detect SAMHD1-mediated hydrolysis of NRTI-triphosphates, verifying that the reduced sensitivi

192 s either reduce RT-mediated incorporation of NRTI triphosphates (discrimination mechanism) or confer

193 The number of NRTI mutations was significantly associated with a highe

194 ellular metabolism and antiviral activity of NRTIs in human peripheral blood mononuclear (PBM) cells

195 hypothesis, we have determined the effect of NRTIs on the expression of proinflammatory cytokines in

196 ther SAMHD1 directly affects the efficacy of NRTIs in inhibiting HIV-1.

197 HIV-1 salvage therapy can safely omit NRTIs without compromising efficacy or durability of res

198 ting a new optimized regimen can safely omit NRTIs without compromising virologic efficacy.

199 No deaths occurred in the omit-NRTIs group compared with 7 deaths in the add-NRTIs grou

200 ity of regimen failure was 29.8% in the omit-NRTIs group versus 25.9% in the add-NRTIs group (differe

201 Omitting NRTIs will reduce pill burden, cost, and toxicity in thi

202 at first drug change and analysis focused on NRTI changes only.

203 ed to NRTI and from HIV-infected patients on NRTI-containing cART.

204 0.03, 1.15) for patients with NNRTI-RAMs or NRTI-RAMs only respectively vs. those without RAMs (p =

205 e to zidovudine, with little impact on other NRTI.

206 (3'-azido-3'-deoxythymidine (AZT)) and other NRTIs is conferred by mutations affecting nucleotide dis

207 nd DNA primers terminated with AZT and other NRTIs, when complexed with RNA or DNA templates.

208 ; p=0.003 versus the protease inhibitor plus NRTI group at 144 weeks.

209 (86%) of 367 in the protease inhibitor plus NRTI group had viral loads of less than 400 copies per m

210 cian-selected NRTIs (protease inhibitor plus NRTI group), protease inhibitor plus raltegravir (400 mg

211 ed no advantage over protease inhibitor plus NRTI in virological efficacy or safety.

212 ndation for ritonavir-boosted lopinavir plus NRTI for second-line antiretroviral therapy.

213 ilpivirine 25 mg or continued efavirenz plus NRTIs for an additional 72 weeks.

214 ld be non-inferior to boosted lopinavir plus NRTIs for virological suppression in resource-limited se

215 istance testing might not accurately predict NRTI activity in protease inhibitor-based second-line AR

216 Over all follow-up, greater predicted NRTI activity was associated with worse viral load suppr

217 characterize the spectrum of low-prevalence NRTI-resistance mutations in HBV obtained from 20 plasma

218 One-half of subjects received NRTIs without expected antiviral activity.

219 PBMCs from HIV-infected patients receiving NRTI-containing cART (n = 39) had significantly lower te

220 ivated CD4(+) T cells only minimally reduced NRTI efficacy.

221 A structurally related NRTI, 2',3'-didehydro-2',3'-dideoxythymidine, is the onl

222 Multiple approved and clinically relevant NRTIs prevented caspase-1 activation, the effector of th

223 Several nucleoside analogue RTIs (NRTIs) blocked K103 RT activity and consistently inhibit

224 lopinavir-ritonavir) plus clinician-selected NRTIs (NRTI group, 426 patients), a protease inhibitor p

225 er day) plus two or three clinician-selected NRTIs (protease inhibitor plus NRTI group), protease inh

226 twice daily), plus two investigator-selected NRTIs (at least one fully active based on resistance tes

227 ry, baseline viral load, nutritional status, NRTIs used, receipt of single-dose nevirapine, and treat

228 Our results showed that NRTI administration up-regulated cytokines, including IL

229 In addition, we found that NRTIs also up-regulated Wnt5a protein.

230 We found that NRTIs inhibit P2X7-mediated NLRP3 inflammasome activatio

231 Our findings suggest that NRTIs are ripe for drug repurposing in P2X7-driven disea

232 These results together suggest that NRTIs up-regulate proinflammatory cytokines via a Wnt5a

233 The NRTI drugs that are used in combinations have different

234 ng RT inhibitor retains activity against the NRTI-resistant mutants K65R and M184V, demonstrating a d

235 n, the merits of switching to FTC/TDF as the NRTI backbone are unknown.

236 women in the PI group than 263 women in the NRTI group (21.4% vs 11.8%, P = .003).

237 in the raltegravir group and 81 (32%) in the NRTI group had grade 3 or higher adverse events; 19 (7%)

238 ants in the raltegravir group and one in the NRTI group were excluded from analyses because of inelig

239 e (46 in the raltegravir group and 50 in the NRTI group).

240 ted during the breast-feeding period (in the NRTI group).

241 to 2.2): 6 were infected in utero (4 in the NRTI group, 1 in the protease-inhibitor group, and 1 in

242 dverse events occurred in 2% of women in the NRTI group, 2% of women in the protease-inhibitor group,

243 of the patients (mean, 255 patients) in the NRTI group, 64% of the patients (mean, 277) in the ralte

244 ies per milliliter in 86% of patients in the NRTI group, 86% in the raltegravir group (P=0.97), and 6

245 ong the three groups at delivery (96% in the NRTI group, 93% in the protease-inhibitor group, and 94%

246 ughout the breast-feeding period (92% in the NRTI group, 93% in the protease-inhibitor group, and 95%

247 altegravir group and 12.4% (8.3-16.5) in the NRTI group, with a weighted difference of -3.4% (-8.4 to

248 e the ultimate effect, the resistance of the NRTI to removal from the genome must be considered, whic

249 nces in virologic efficacy, according to the NRTI combination, among patients with screening HIV-1 RN

250 260 to the raltegravir group and 255 to the NRTI group; two participants in the raltegravir group an

251 vant drug interactions-coformulated with the NRTI combination emtricitabine and tenofovir alafenamide

252 ir group (P=0.21 for the comparison with the NRTI group; superiority of raltegravir not shown), and 5

253 The NRTIs emtricitabine [(-)-2,3'-dideoxy-5-fluoro-3'-thiacy

254 The NRTIs zidovudine (AZT), stavudine (d4T), didanosine (ddI

255 agnosis and hospital admission by use of the NRTIs tenofovir disoproxil fumarate (TDF)/emtricitabine

256 ity, predicted by resistance testing, of the NRTIs used in second-line therapy and treatment outcomes

257 Removing the NRTIs or replacing them with raltegravir may provide a b

258 a protease inhibitor in second-line therapy, NRTIs retained substantial virologic activity without ev

259 itonavir-boosted lopinavir plus two or three NRTIs selected from an algorithm (eg, zidovudine after f

260 tonavir-boosted lopinavir) with two to three NRTIs (clinician-selected, without resistance testing);

261 reases the sensitivity of mammalian cells to NRTI exposure by reducing mitochondrial function.

262 utations that were reported to contribute to NRTI resistance in HIV-1.

263 in PBMCs from uninfected patients exposed to NRTI and from HIV-infected patients on NRTI-containing c

264 Some level of susceptibility to NRTI remained; however, VL monitoring and earlier virolo

265 ing that the reduced sensitivity of HIV-1 to NRTIs upon SAMHD1 degradation is most likely caused by t

266 exists regarding the resistance of HIV-2 to NRTIs.

267 ingle class TDR was 10.0%, 5.1%, and 1.6% to NRTIs, NNRTIs, and PIs.

268 nterestingly, two subjects had major DRMs to NRTIs, NNRTIs, and 4 mutations in the Gag P2/NC CS.

269 ribed the development of HIV-1 resistance to NRTIs and identified mutations in the polymerase domain

270 ng the molecular mechanisms of resistance to NRTIs and NNRTIs, and their complex relationships, may h

271 Triple-class resistance to NRTIs, NNRTIs, and PR inhibitors was observed in 24 (53%

272 nces between Pol gamma and RT in response to NRTIs will provide invaluable insight to aid in designin

273 ese mutations cause increased sensitivity to NRTIs, such as AZT.

274 ravir was non-inferior, but not superior, to NRTIs.

275 Findings show that in Lilongwe TDR to NRTIs and PIs was <5%, whereas TDR to NNRTIs was 5%-15%.

276 As a result, (-)-FTC is a much less toxic NRTI.

277 s achieving <=50% suppression of transmitted NRTI resistance.

278 Among people with transmitted NRTI resistance (5.8%), baseline genotype guides NRTI se

279 NRTI triphosphates (NRTI-TP), the biologically active forms, act as chain te

280 NRTI-triphosphates (NRTI-TP) compete with endogenous 2'-deoxyribonucleosides

281 t-line treatment containing an NNRTI and two NRTIs, had virological failure (confirmed HIV-1 RNA >=40

282 rse transcriptase inhibitor (NNRTI) plus two NRTIs has failed.

283 The two NRTIs escape some of the active site selection through t

284 When administered with two NRTIs, dolutegravir was superior to ritonavir-boosted lo

285 Unfortunately, NRTIs also inhibit human mitochondrial DNA polymerase (P

286 tter than any of the current clinically used NRTIs.

287 ht of increasing resistance to commonly used NRTIs in global HIV treatment programs, targeting nucleo

288 and restore susceptibility of commonly used NRTIs.

289 inhibits viral vectors that replicate using NRTI-resistant HIV-1 RTs, and there is no obvious toxici

290 antly decreases HIV-1 sensitivity to various NRTIs in macrophages.

291 after failure with tenofovir and vice versa; NRTI group).

292 subtype AE) from Thailand; all subjects were NRTI naive.

293 tion may mediate the effects of HIV, whereas NRTIs likely mediate the effects of ART.

294 cy virus type 1 (HIV-1) infection, but which NRTI combination has greater efficacy and safety is not

295 3 (61.5%) with NNRTI-RAMs, 7/11 (63.6%) with NRTI-RAMs only, and 51/59 (86.4%) without RAMs.

296 transcriptase (RT) mutation associated with NRTI and NNRTI resistance, respectively.

297 (pol gamma), which is often associated with NRTI toxicity, as well as the viral target protein, WT H

298 lood mononuclear cells (PBMCs) cultured with NRTI and ex vivo in PBMCs from uninfected patients expos

299 NA abundance and mitochondrial function with NRTI treatment.

300 ident diabetes is 33% lower in patients with NRTI exposure among 128,861 patients with HIV-1 or hepat

301 ignificantly lower CD4 cells than those with NRTI-DRMs on ART (p = 0.042).

302 PS detected low-prevalence HBV variants with NRTI-resistance mutations, G-to-A hypermutation, and low

303 A regimen of protease inhibitor with NRTIs remains the best standardised second-line regimen