ライフサイエンスコーパス: NRTI

1 NRTI phosphorylation seems to correlate with mitochondri

2 NRTI resistance-associated mutations were reported in fo

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

4 NRTI triphosphates, the active moieties, inhibit human i

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

6 NRTIs abrogated functional effects of transgenically inc

7 NRTIs and, specifically tenofovir at therapeutic concent

8 NRTIs based on the carbocyclic pseudosugar may offer an

9 NRTIs increased left ventricle mass 20% in TK2 TGs.

10 NRTIs were efficacious in mouse models of geographic atr

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

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

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

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

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

16 infected with HIV and were receiving > or =2 NRTIs, to determine the relative toxicities of the 5 mos

17 itial regimens consisting of an InSTI plus 2 NRTIs.

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

19 bitors or boosted protease inhibitors with 2 NRTIs.

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

21 zed to treatment groups that received 2 or 3 NRTIs with efavirenz.

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

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

24 regimen of NRTIs + lopinavir/ritonavir, or a NRTI-sparing regimen of efavirenz + lopinavir/ritonavir.

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

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

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

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

29 77%) of 26 patients with two or three active NRTIs had viral suppression (p=0.08).

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 en versus regimens that included EFV plus an NRTI.

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

39 treat HIV-1 infections, nucleoside analogs (NRTIs) and nonnucleosides (NNRTIs), and there are promis

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

41 nd laboratory toxicities were estimated, and NRTI pairs were compared with regard to the time to the

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

45 n the mechanism of synergy between NNRTI and NRTI.

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

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

48 sm of action that is different from approved NRTIs.

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

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

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

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

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

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

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

56 Estimates differed by NRTI backbone.

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

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

59 osphorylation by TK2 is integral to clinical NRTI mitochondrial toxicity.

60 the relative toxicities of the 5 most common NRTI pairs: zidovudine (ZDV)/lamivudine (3TC), ZDV/didan

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

62 virine, respectively, independent of current NRTI backbones.

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

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

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

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

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

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

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

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

71 c failure, compared with efavirenz plus dual NRTIs.

72 VCV administered with dual NRTIs in treatment-naive subjects with HIV-1 infection h

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

74 up), and lopinavir-ritonavir plus efavirenz (NRTI-sparing group).

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

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

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

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

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

80 %) subjects: 10 (18%) for NNRTIs, 2 (4%) for NRTIs, and 3 (5.5%) for PIs.

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

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

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

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

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

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

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

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

89 nucleoside reverse transcriptase inhibitor (NRTI) backbone.

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

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

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

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

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

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

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

97 nucleoside reverse-transcriptase inhibitor (NRTI) regimen versus regimens that included EFV plus an

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

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

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

101 nucleoside reverse transcriptase inhibitor (NRTI) selection.

102 nucleoside reverse transcriptase inhibitor (NRTI) therapy.

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

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

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

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

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

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

109 bitors (NNRTI) and nucleoside RT inhibitors (NRTIs) is due to inhibition by the NNRTI of the rate at

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

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

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

113 nucleoside reverse transcriptase inhibitors (NRTIs and NNRTIs).

114 nucleoside reverse transcriptase inhibitors (NRTIs and NNRTIs).

115 nucleoside reverse transcriptase inhibitors (NRTIs) + efavirenz, a non-nucleoside reverse transcripta

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

117 nucleoside reverse transcriptase inhibitors (NRTIs) and efavirenz in patients with higher viral loads

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

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

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

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

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

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

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

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

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

127 nucleoside reverse transcriptase inhibitors (NRTIs) for acquired immune deficiency syndrome.

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

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

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

131 nucleoside reverse-transcriptase inhibitors (NRTIs) in the treatment-naive HIV-1-infected subjects.

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

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

134 nucleoside reverse-transcriptase inhibitors (NRTIs) is recommended for initial therapy for patients w

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

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

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

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

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

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

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

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

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

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

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

146 nucleoside reverse-transcriptase inhibitors (NRTIs).

147 nucleoside reverse transcriptase inhibitors (NRTIs).

148 nucleoside reverse-transcriptase inhibitors (NRTIs).

149 nucleoside reverse-transcriptase inhibitors (NRTIs).

150 nucleotide reverse transcriptase inhibitors (NRTIs).

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

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

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

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

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

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

157 predicted activity of prescribed second-line NRTIs.

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

159 ologic failure detection may result in lower NRTI resistance.

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

161 These compounds are effective against many NRTI drug-resistant RT variants; however, the M184V muta

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

163 mpeding the development of excision-mediated NRTI resistance.

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

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

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

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

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

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

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

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

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

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

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

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

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

177 Absence of NRTI mutations and subtherapeutic ART preswitch were ass

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

179 ratory abnormality before discontinuation of NRTI assignment.

180 ys simultaneously may delay the emergence of NRTI resistance and prolong treatment response.

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

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

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

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

185 ism between the K65R and T215Y/F pathways of NRTI resistance occurs at the genomic level.

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

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

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

189 IV-1 RT facilitates ATP-mediated excision of NRTIs from chain-terminated template/primers (T/P).

190 e transcriptase inhibitor-sparing regimen of NRTIs + lopinavir/ritonavir, or a NRTI-sparing regimen o

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

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

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

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

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

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

197 0.03, 1.15) for patients with NNRTI-RAMs or NRTI-RAMs only respectively vs. those without RAMs (p =

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

199 (3'-azido-3'-deoxythymidine (AZT)) and other NRTIs is conferred by mutations affecting nucleotide dis

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

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

202 (86%) of 367 in the protease inhibitor plus NRTI group had viral loads of less than 400 copies per m

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

220 TK2 and cytoplasmic TK1) were used to study NRTI mitochondrial toxicity.

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

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

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

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

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

226 The NRTI drugs that are used in combinations have different

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

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

229 n important role for RNase H activity in the NRTI excision phenotype and in the mechanism of synergy

230 s an important role for this activity in the NRTI excision phenotype.

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

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

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

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

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

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

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

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

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

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

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

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

243 he lopinavir-ritonavir group, and 83% in the NRTI-sparing group (P=0.003 for the comparison between t

244 ) but was not significantly different in the NRTI-sparing group from the time in either of the other

245 sistance mutations were more frequent in the NRTI-sparing group than in the other two groups.

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

247 The virologic efficacy of the NRTI-sparing regimen was similar to that of the efaviren

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

249 260 to the raltegravir group and 255 to the NRTI group; two participants in the raltegravir group an

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

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

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

253 The NRTIs were lamivudine + stavudine, zidovudine, or tenofo

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

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

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

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

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

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

260 Thus, NRTI mitochondrial phosphorylation by TK2 is integral to

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

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

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

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

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

278 mens for initial therapy: efavirenz plus two NRTIs (efavirenz group), lopinavir-ritonavir plus two NR

279 avirenz group), lopinavir-ritonavir plus two NRTIs (lopinavir-ritonavir group), and lopinavir-ritonav

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

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

282 tter than any of the current clinically used NRTIs.

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

284 and restore susceptibility of commonly used NRTIs.

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

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

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

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

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

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

291 3 (61.5%) with NNRTI-RAMs, 7/11 (63.6%) with NRTI-RAMs only, and 51/59 (86.4%) without RAMs.

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

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

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

295 NA abundance and mitochondrial function with NRTI treatment.

296 Therapy with NRTI combinations that select both pathways simultaneous

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

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

299 Toxicities associated with NRTIs are not fully defined in children.

300 nz may prevent toxic effects associated with NRTIs.

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