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1 e transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors).
2 tase inhibitors (NRTIs) and a non-nucleoside reverse transcriptase inhibitor.
3 ncoming viral RNAs even in the presence of a reverse transcriptase inhibitor.
4 on a first-generation nonnucleoside analogue reverse transcriptase inhibitor.
5 4-5.9]); all mutations were to nonnucleoside reverse transcriptase inhibitors.
6 viously described for the IAS non-nucleoside reverse transcriptase inhibitors.
7 ved 400 mg RAL twice daily plus 2 nucleoside reverse transcriptase inhibitors.
8 ders viral resistance to multiple nucleoside reverse transcriptase inhibitors.
9 late the prophylactic efficacy of nucleotide reverse transcriptase inhibitors.
10 ing of at least two nucleoside or nucleotide reverse transcriptase inhibitors.
11 without evidence of resistance to nucleoside reverse transcriptase inhibitors.
12 ict PrEP potency for all drug classes except reverse transcriptase inhibitors.
13 rs (PI) with the same backbone of Nucleoside Reverse Transcriptase Inhibitors.
14 l antiretroviral therapy with two nucleoside reverse transcriptase inhibitors.
15 he DNA-DSB site, and TSIs were suppressed by reverse-transcriptase inhibitors.
16 e-transcriptase inhibitors and nonnucleoside reverse-transcriptase inhibitors.
17 iation (0.71 [0.61-0.82]) and non-nucleoside reverse transcriptase inhibitor (0.68 [0.51-0.90]) or in
18 of two pyrimidine-based HIV-1 non-nucleoside reverse transcriptase inhibitors, 1 (MC1501) and 2 (MC20
20 Quantification of 6 nucleoside/nucleotide reverse transcriptase inhibitors, 2 non-nucleoside rever
21 eekly CD4 counts and to receive 2 nucleoside reverse transcriptase inhibitors (2NRTI, mainly abacavir
22 on for NNRTIs (5.4%), followed by nucleoside reverse transcriptase inhibitors (3.0%) and protease inh
24 criptase inhibitor (NRTI) plus nonnucleoside reverse-transcriptase inhibitor (43%), NRTI plus integra
26 e transcriptase inhibitors, 2 non-nucleoside reverse transcriptase inhibitors, 7 protease inhibitors,
27 o major mutations (3% vs 51%), nonnucleoside reverse transcriptase inhibitor (94% vs 44%), M184V/I (9
28 larly in the quantification of nonnucleoside reverse transcriptase inhibitor and lamivudine mutations
29 newer PIs, second-generation non-nucleoside reverse transcriptase inhibitors and drugs in novel clas
31 in the cART regimen, in favor of nucleoside reverse transcriptase inhibitors and integrase inhibitor
32 ce; 1 EFV, emergent resistance to nucleoside reverse transcriptase inhibitors and nonnucleoside rever
36 ied as moderate (5%-15%) for both nucleoside reverse-transcriptase inhibitors and nonnucleoside rever
37 ther multitarget therapy with enfuvirtide, 2 reverse-transcriptase inhibitors, and a ritonavir-booste
38 resistance, background regimen of nucleoside reverse-transcriptase inhibitors, and the standard ramp-
39 reverse transcriptase inhibitor-, nucleoside reverse transcriptase inhibitor-, and protease inhibitor
40 our detection specificity with the use of a reverse transcriptase inhibitor as a counterscreen, enab
41 ntification of thymidine analogue nucleoside reverse transcriptase inhibitors as the cause of lipoatr
42 core </=2 in 10 patients included nucleoside reverse transcriptase inhibitors associated with darunav
43 imilar proportions of overall and nucleoside reverse transcriptase inhibitor-associated minority vari
44 ipant in the atazanavir group had nucleoside reverse transcriptase inhibitor-associated resistance th
46 e implicated in susceptibility to nucleoside reverse-transcriptase inhibitor-associated toxicity.
47 he clinically administered nucleoside analog reverse transcriptase inhibitor azidothymidine (AZT).
50 of virologic failure with either nucleoside reverse transcriptase inhibitor backbone than women assi
51 a boosted darunavir regimen with nucleoside reverse transcriptase inhibitor background treatment for
54 lopinavir/ritonavir (LPV/r) or nonnucleoside reverse transcriptase inhibitor-based ART and treated wi
56 1.01-1.07), being prescribed non-nucleoside reverse transcriptase inhibitor-based regimens (1.63, 1.
57 nce interval [CI], 90%-99.7%); nonnucleoside reverse transcriptase inhibitor-based, 100% (95% CI, 91%
58 use of a tenofovir-containing nonnucleoside reverse-transcriptase inhibitor-based first-line regimen
60 Antihepadnaviral treatment using an approved reverse transcriptase inhibitor blocked replication of a
61 dence that telomerase can add the nucleotide reverse transcriptase inhibitors ddITP and AZT-TP to the
62 localization of LysRS, but treatment with a reverse transcriptase inhibitor does not, suggesting tha
63 AS, or treatment of MAVS-deficient mice with reverse transcriptase inhibitors, dramatically inhibits
68 tance to older thymidine analogue nucleoside reverse transcriptase inhibitor drugs has been identifie
69 eiving tenofovir prodrugs, the nonnucleoside reverse transcriptase inhibitors efavirenz and rilpiviri
70 vitegravir, or raltegravir), a nonnucleoside reverse transcriptase inhibitor (efavirenz or rilpivirin
71 or abacavir/lamivudine) plus a nonnucleoside reverse transcriptase inhibitor (efavirenz), a ritonavir
73 ART regimens based on either Non-Nucleoside Reverse Transcriptase Inhibitors (EFV) or ritonavir-boos
74 , both with investigator-selected nucleoside reverse transcriptase inhibitors: emtricitabine and teno
78 rhesus macaques with protease, integrase, or reverse transcriptase inhibitors for 1 to 2 or for 5 to
81 -retroviral therapy with multiple nucleoside reverse transcriptase inhibitors for the treatment of pa
82 n inhibitor (PIE12-Trimer), a combination of reverse transcriptase inhibitors (FTC-TDF), a thioester
83 n that combined nucleoside and nonnucleoside reverse-transcriptase inhibitors (hereafter, "NNRTI stra
84 bserved with other non-allergenic nucleoside reverse transcriptase inhibitors, identifying abacavir a
85 anscriptase inhibitors in 62%, nonnucleoside reverse transcriptase inhibitors in 57%, protease inhibi
86 9 youth, identified resistance to nucleoside reverse transcriptase inhibitors in 62%, nonnucleoside r
87 sted proteasome inhibitors and nonnucleotide reverse transcriptase inhibitors in the cART regimen, in
88 pregnancy, 1 of which was without nucleoside reverse transcriptase inhibitors, infants had a specific
89 these new features with a simple case (HIV-1 reverse transcriptase/inhibitor interaction) and with th
90 ontaining dapivirine, a non-nucleoside HIV-1 reverse-transcriptase inhibitor, involving women between
92 as 2-LTR quantification and the addition of reverse transcriptase inhibitors, is crucial to fully el
94 Treatment of aged mice with the nucleoside reverse transcriptase inhibitor lamivudine downregulated
95 resistance to the co-administered nucleoside reverse transcriptase inhibitors might reduce effectiven
96 e (RPV) and EFV plus 2 nucleoside/nucleotide reverse transcriptase inhibitors (N[t]RTIs) in treatment
100 lopinavir and saquinavir, the nonnucleoside reverse-transcriptase inhibitor nevirapine, and the anti
101 (darunavir, atazanavir), and 2 nonnucleoside reverse transcriptase inhibitors (nevirapine, efavirenz)
102 avirenz is a second-generation nonnucleoside reverse transcriptase inhibitor (NNRTI) and a common com
103 luated for drug resistance to non-nucleoside reverse transcriptase inhibitor (NNRTI) at codons Lys103
105 "switch region" and the viral non-nucleoside reverse transcriptase inhibitor (NNRTI) binding site.
106 led RT in the presence of the non-nucleoside reverse transcriptase inhibitor (NNRTI) efavirenz (EFV)
107 ated that a formulation of the nonnucleoside reverse transcriptase inhibitor (NNRTI) MIV-150 in carra
108 mutations (4.5%), followed by nonnucleoside reverse transcriptase inhibitor (NNRTI) mutations (2.9%)
109 y abacavir+lamivudine) with a non-nucleoside reverse transcriptase inhibitor (NNRTI) or 3 NRTIs as lo
110 psychiatric side-effects on a non-nucleoside reverse transcriptase inhibitor (NNRTI) or who are on a
111 antiretroviral therapy with a non-nucleoside reverse transcriptase inhibitor (NNRTI) plus two NRTIs h
112 eficiency virus type 1 (HIV-1) nonnucleoside reverse transcriptase inhibitor (NNRTI) resistance mutat
113 ttributable to an increase in non-nucleoside reverse transcriptase inhibitor (NNRTI) resistance.
114 e risk factors associated with nonnucleoside reverse transcriptase inhibitor (NNRTI) resistance.
117 leoside human immunodeficiency virus (HIV)-1 reverse transcriptase inhibitor (NNRTI), was safe and ef
118 mg every 48 hours as part of a nonnucleoside reverse transcriptase inhibitor (NNRTI)- or lopinavir/ri
119 protease inhibitor (PI)-, and nonnucleoside reverse transcriptase inhibitor (NNRTI)-based ART betwee
121 n protease inhibitor (PI)- and nonnucleoside reverse transcriptase inhibitor (NNRTI)-based regimens w
122 rologic failure for first-line nonnucleoside reverse transcriptase inhibitor (NNRTI)-based regimens.
126 ne/efavirenz, presence of both nonnucleoside reverse transcriptase inhibitor (NNRTI)/nucleoside rever
127 ) or on a regimen containing a nonnucleoside reverse transcriptase inhibitor (NNRTI; N = 52) or prote
128 dine or emtricitabine) plus a non-nucleoside reverse transcriptase inhibitor (NNRTI; nevirapine or ef
129 of alkenyldiarylmethane (ADAM) nonnucleoside reverse transcriptase inhibitors (NNRTI) 3 and 4 with HI
130 ountries are moving away from non-nucleoside reverse transcriptase inhibitors (NNRTI) and transitioni
131 tice regarding the use of the non-nucleoside reverse transcriptase inhibitors (NNRTI) efavirenz (EFV)
132 al increases in resistance to non-nucleoside reverse transcriptase inhibitors (NNRTI) in east Africa
134 n than protease inhibitors or non-nucleoside reverse transcriptase inhibitors (NNRTI), with dolutegra
135 aluated the impact of several non-nucleoside reverse transcriptase inhibitors (NNRTI; Efavirenz, Etra
136 table markedly faster than did nonnucleoside reverse-transcriptase inhibitor (NNRTI) mutations (hazar
137 ed patients failing an initial nonnucleoside reverse-transcriptase inhibitor (NNRTI) regimen in Afric
138 over increasing prevalence of non-nucleoside reverse-transcriptase inhibitor (NNRTI) resistance in pe
139 or (NRTI) resistance, 9.8% had nonnucleoside reverse-transcriptase inhibitor (NNRTI) resistance, and
140 Doravirine (DOR), a novel non-nucleoside reverse-transcriptase inhibitor (NNRTI), is active again
141 llows: exposure to nonstandard nonnucleoside reverse-transcriptase inhibitor (NNRTI)-based (hazard ra
143 ing of ART as a change from a non-nucleoside reverse-transcriptase inhibitor (NNRTI)-based regimen to
144 patients initiating first-line nonnucleoside reverse-transcriptase inhibitor (NNRTI)-based therapy su
145 ling therapy on a TDF/XTC plus nonnucleoside reverse-transcriptase inhibitor (NNRTI)-containing regim
146 We sought to detect minor nonnucleoside reverse-transcriptase inhibitor (NNRTI)-resistant varian
147 ffect of pre-existing minority nonnucleoside reverse-transcriptase inhibitor (NNRTI)-resistant varian
148 40%), boosted ARVs (30%), and non-nucleoside reverse transcriptase inhibitors (NNRTIs) (32%) based re
149 riptase inhibitors (NRTIs), 4 non-nucleoside reverse transcriptase inhibitors (NNRTIs) and 2 protease
153 riptase inhibitors (NRTIs) and nonnucleoside reverse transcriptase inhibitors (NNRTIs) has been assoc
154 he prevalence of resistance to nonnucleoside reverse transcriptase inhibitors (NNRTIs) have been obse
157 lence levels of resistance to non-nucleoside reverse transcriptase inhibitors (NNRTIs) measured in th
158 iral therapy (ART) containing non-nucleoside reverse transcriptase inhibitors (NNRTIs) might compromi
160 e prevalence of resistance to non-nucleoside reverse transcriptase inhibitors (NNRTIs) reached 45% (9
162 Rising resistance of HIV-1 to non-nucleoside reverse transcriptase inhibitors (NNRTIs) threatens the
163 ation of a clinical candidate non-nucleoside reverse transcriptase inhibitors (NNRTIs) with a novel a
164 nscriptase inhibitors (NRTIs), nonnucleoside reverse transcriptase inhibitors (NNRTIs), and protease
165 (1H)-ones were synthesized as non-nucleoside reverse transcriptase inhibitors (NNRTIs), and their bio
166 nd tallied major mutations to non-nucleoside reverse transcriptase inhibitors (NNRTIs), nucleoside re
167 itted drug resistance (TDR) to nonnucleoside reverse transcriptase inhibitors (NNRTIs), nucleoside re
168 , is influenced by mutations, non-nucleoside reverse transcriptase inhibitors (NNRTIs), nucleotide su
169 an were protease inhibitors or nonnucleoside reverse transcriptase inhibitors (NNRTIs), with dolutegr
173 riptase inhibitors [NRTIs] and nonnucleoside reverse transcriptase inhibitors [NNRTIs]), integrase st
174 in patients receiving PIs and nonnucleoside reverse transcriptase inhibitors [NNRTIs], and 60.3% [P
175 Here, we assessed the ability of nucleoside reverse-transcriptase inhibitor/nonnucleoside reverse-tr
176 ritonavir-boosted lopinavir and a nucleoside reverse transcriptase inhibitor (NRTI) backbone among th
177 fumarate (FTC/TDF) is a preferred nucleoside reverse transcriptase inhibitor (NRTI) backbone with lam
179 iated ART consisting of different nucleoside reverse transcriptase inhibitor (NRTI) backbones (zidovu
180 ns (47% vs 18%), all P = .01; and nucleoside reverse transcriptase inhibitor (NRTI) cross-resistance
181 MS-986001 is a thymidine analogue nucleoside reverse transcriptase inhibitor (NRTI) designed to maint
182 SPNs) of the highly water-soluble nucleoside reverse transcriptase inhibitor (NRTI) emtricitabine (FT
183 ine or emtricitabine plus another nucleoside reverse transcriptase inhibitor (NRTI) in fixed-dose com
184 apy (ART) for HIV patients is the nucleoside reverse transcriptase inhibitor (NRTI) is tenofovir.
185 of greater emergence of the K65R nucleoside reverse transcriptase inhibitor (NRTI) mutation in human
186 t frequent indicators of TDR were nucleoside reverse transcriptase inhibitor (NRTI) mutations (4.5%),
187 individuals; 15.8% had nucleoside/nucleotide reverse transcriptase inhibitor (NRTI) resistance, 9.8%
191 S-p53 cells were treated with the nucleoside reverse transcriptase inhibitor (NRTI), 2',3'-dideoxycyt
192 , HIV-positive patients receiving nucleoside reverse transcriptase inhibitor (NRTI)-based ART, and HI
195 inhibitor mutations; 41 (91%) had nucleoside reverse-transcriptase inhibitor (NRTI) mutations; 33 (73
196 mmon ART regimens were nucleoside/nucleotide reverse-transcriptase inhibitor (NRTI) plus nonnucleosid
197 namics of emerging nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI) resistance in hep
198 V) alone is attractive because of nucleoside reverse-transcriptase inhibitor (NRTI)-sparing benefits,
200 , zidovudine, and lamivudine (the nucleoside reverse-transcriptase inhibitor [NRTI] group) or lopinav
201 o two classes: nucleoside and non-nucleoside reverse transcriptase inhibitors (NRTIs and NNRTIs).
202 l resistance to nucleoside and nonnucleoside reverse transcriptase inhibitors (NRTIs and NNRTIs).
203 18 years who started ART with two nucleoside reverse transcriptase inhibitors (NRTIs) and a non-nucle
204 first-line regimen of PI/r plus 2 nucleoside reverse transcriptase inhibitors (NRTIs) and had at leas
206 development of drug resistance to nucleoside reverse transcriptase inhibitors (NRTIs) and nonnucleosi
209 ministered with two nucleoside or nucleotide reverse transcriptase inhibitors (NRTIs) are recommended
212 of the OPTIONS trial showed that nucleoside reverse transcriptase inhibitors (NRTIs) can be safely o
213 irenz 600 mg once a day with dual nucleoside reverse transcriptase inhibitors (NRTIs) for 24 weeks of
214 (Ed4T), have been investigated as nucleoside reverse transcriptase inhibitors (NRTIs) for treatment o
215 navir-boosted lopinavir, plus two nucleoside reverse transcriptase inhibitors (NRTIs) in adults in wh
216 the potency of nucleoside/nucleotide analog reverse transcriptase inhibitors (NRTIs) is an important
217 opinavir, and atazanavir) but not nucleoside reverse transcriptase inhibitors (NRTIs) or nonnucleosid
218 regimens for most patients are 2 nucleoside reverse transcriptase inhibitors (NRTIs) plus an integra
219 taggered interruption, whereby nucleos(t)ide reverse transcriptase inhibitors (NRTIs) were continued
222 ranscriptase inhibitors (NNRTIs), nucleoside reverse transcriptase inhibitors (NRTIs), and protease i
223 ranscriptase inhibitors (NNRTIs), nucleoside reverse transcriptase inhibitors (NRTIs), and protease i
224 ization method to classify TDR to nucleoside reverse transcriptase inhibitors (NRTIs), nonnucleoside
228 mended initial regimens include 2 nucleoside reverse transcriptase inhibitors (NRTIs; abacavir/lamivu
229 The efficacy and toxic effects of nucleoside reverse-transcriptase inhibitors (NRTIs) are uncertain w
230 o paediatric trials have compared nucleoside reverse-transcriptase inhibitors (NRTIs) in first-line a
231 is expected to impair activity of nucleoside reverse-transcriptase inhibitors (NRTIs) in second-line
233 ndard protease inhibitor plus two nucleoside reverse-transcriptase inhibitors (NRTIs) second-line com
234 The use of fixed-dose combination nucleoside reverse-transcriptase inhibitors (NRTIs) with a nonnucle
235 Subjects received nucleoside or nucleotide reverse-transcriptase inhibitors (NRTIs) with or without
236 o 12 HIV-1 inhibitors including 6 nucleoside reverse-transcriptase inhibitors (NRTIs), 4 non-nucleosi
239 reverse transcriptase inhibitors (nucleoside reverse transcriptase inhibitors [NRTIs] and nonnucleosi
240 and cohorts B (B1, best available nucleoside reverse transcriptase inhibitors [NRTIs] plus ritonavir-
241 y associated with a nucleoside or nucleotide reverse transcriptase inhibitor (NtRTI)-sparing regimen.
242 ease inhibitor plus nucleoside or nucleotide reverse transcriptase inhibitors (NtRTIs) might be compr
243 ection includes two nucleoside or nucleotide reverse transcriptase inhibitors (NtRTIs), but these dru
244 ated with resistance to protease inhibitors, reverse transcriptase inhibitors (nucleoside reverse tra
245 o against wild-type HIV-1 and non-nucleoside reverse transcriptase inhibitor-, nucleoside reverse tra
246 Here we analyzed whether abacavir, an HIV-1 reverse transcriptase inhibitor often inducing severe de
248 her effective regimens include nonnucleoside reverse transcriptase inhibitors or boosted protease inh
249 d first-line regimens based on nonnucleoside reverse transcriptase inhibitors or integrase inhibitors
250 tase inhibitors (NRTIs) with a nonnucleoside reverse-transcriptase inhibitor or a ritonavir-boosted p
251 therapy (ART) with at least 1 nonnucleoside reverse-transcriptase inhibitor or protease inhibitor.
252 but not among mothers who used nonnucleoside reverse-transcriptase inhibitor or triple-nucleoside reg
253 RNA from HIV-1-infected cells treated with a reverse-transcriptase inhibitor or with heat-inactivated
254 e transcriptase inhibitor (NNRTI)/nucleoside reverse transcriptase inhibitor PDR vs no PDR was associ
256 ical responses to cART based on 2 nucleoside reverse transcriptase inhibitors plus 1 ritonavir-booste
257 The regimen consisted of two nucleoside reverse transcriptase inhibitors plus nevirapine dosed a
258 criptase inhibitors (NRTIs) or nonnucleoside reverse transcriptase inhibitors reduced trophoblast pro
261 e (63%) of eight had archived non-nucleoside reverse transcriptase inhibitor resistance-associated mu
262 icipants with HIV-1 infection, nonnucleoside reverse-transcriptase inhibitor resistance mutations wer
265 two decades since the approval of the first reverse transcriptase inhibitor (retrovir, GlaxoSmithKli
266 long-acting formulation of the nonnucleoside reverse transcriptase inhibitor rilpivirine (RPV LA) has
268 eened the efficacy of commercially available reverse transcriptase inhibitors (RTIs) at inhibiting th
269 ested to be a major substrate for TREX1, and reverse transcriptase inhibitors (RTIs) were proposed as
270 the host cells, such as entry inhibitors or reverse transcriptase inhibitors (RTIs), are ideal candi
272 ofile, which support its use as a nucleoside reverse transcriptase inhibitor-sparing and protease inh
273 -1 transmission and/or for use in nucleoside reverse transcriptase inhibitor-sparing antiretroviral r
274 ase inhibitors, nonnucleoside and nucleotide reverse transcriptase inhibitors TDR mutations, namely,
275 fidence interval, 0.07%-13.8%) nonnucleoside reverse-transcriptase inhibitor TDR was determined.
276 nhibitor (PI) lopinavir (LPV) and nucleoside reverse transcriptase inhibitor tenofovir alafenamide (T
277 ntly dosed vaginal gels containing the HIV-1 reverse transcriptase inhibitor tenofovir protected pigt
278 enofovir alafenamide delivers the nucleotide reverse transcriptase inhibitor tenofovir to target cell
280 mended initial regimens include 2 nucleoside reverse transcriptase inhibitors (tenofovir/emtricitabin
284 etroviral medications, such as nonnucleoside reverse transcriptase inhibitors, the detection of these
285 the mechanisms by which nucleoside-analogue reverse transcriptase inhibitors, the most common class
286 ularly among those with mono/dual nucleoside reverse transcriptase inhibitor therapy prior to combina
287 RNA concentration and background nucleoside reverse transcriptase inhibitor therapy, to doravirine (
289 verse-transcriptase inhibitor and nucleoside reverse-transcriptase inhibitor transmitted drug resista
290 everse-transcriptase inhibitor/nonnucleoside reverse-transcriptase inhibitor treatment to restore the
292 ociations between single and dual nucleoside reverse-transcriptase inhibitor use and possible mitocho
293 rdiovascular (CV) toxicity of the nucleoside reverse-transcriptase inhibitors used to treat human imm
295 uring antiretroviral therapy with nucleoside reverse-transcriptase inhibitors was previously associat
296 Relevant mutations affecting nonnucleoside reverse transcriptase inhibitors were found in 32 of 133
297 d efavirenz, were open-label; the nucleoside reverse transcriptase inhibitors were prematurely unblin